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    Biochemistry in the AI Era Special Issue
  • YANG Yi-Xuan, Morigen
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 519-530. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1400
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    Most recently, Quake proposed the “cellular dogma” in which the central dogma, cell theory and theory of evolution should be integrated to understand a major conceptual challenge for biology in the next decade. However, the “cellular dogma” remains to be developed theoretically and experimentally. Quantum biology is an interdisciplinary field to study quantum effects in dynamic structures of biological molecules and energy transfer, and further understand the quantum mechanics of chemical processes and the origin of life by using quantum theories and methods. We wonder whether quantum biology could explain the basic nature of life in the most general sense. Herein, we first provide a brief review on the development of quantum mechanics and the conceptions in quantum biology, then we summarize the present theories of quantum biology and discuss a possible prospectives. We cover the following contents of quantum biology: Quantum tunneling due to a decrease of proton stability by hydrogen bond breakage in DNA replication and repair cause permanent mutations with evolutionary impacts; the tunneling due to conformational short-range motion and static environment optimization in enzyme molecules is found to promote enzymatic reactions by reduction of the effective barrier height; the activated electrons are in a phase-synchronized superposition state between multiple pigment molecules, enhancing the conversion of light energy into chemical energy with high efficiency by optimizing the energy transfer path through phase-length interference; quantum compasses in bird migration lead to sense the way by detecting weak magnetic fields through electron transfer and successive conformational changes in cryptochrome; collapses of conformational state of microtubules in the nervous system due to quantum coherence, superposition, entanglement and Orchestrated Objective Reduction (Orch-OR) collapse can sense and transmit neuro-information. Finally, the paper also discusses the possibilities and prospectives in experimental evidence for quantum mechanical simulation of life activities, whether the “observer effect” may provide new ideas for explaining the origin of life, and whether the Copenhagen interpretation could explain the basic nature of life.
  • WANG Yang, HU Jian
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 531-541. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1504
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    Set against the artificial intelligence (AI)-driven transformation of the educational landscape, this paper discusses how the Molecular Biology course is implementing a question-driven pedagogical reform, centering on fostering innovation as its primary goal. We introduce the educational philosophy of “Co-evolution of Inquiry and Learning”, positing that questioning and knowledge acquisition function as interdependent strands—analogous to DNA’s double helix—mutually catalyzing cognitive development and igniting innovative potential. Guided by this conceptual framework, a comprehensive instructional system has been constructed. At the content level, a three-level question bank (Foundational Cognition-Comprehensive Application-Innovative Exploration) incorporates AI tools to streamline knowledge acquisition, enhance complex problem-solving capabilities,and facilitate cutting-edge research exploration. Methodologically, the four-step teaching method (ContextualQuestioning-Autonomous Inquiry-Collaborative Discussion-Reflective Questioning) systematically activates the question bank through sequenced implementation, enabling students’transition from responding to instructor-initiated questions to generating original inquiries. The formative assessment system examines five dimensions of students’competencies while providing timely diagnostic feedback. Through two years of implementation, this AI-enhanced “inquiry-initiated, mutually reinforcing” pedagogical model has successfully transformed Molecular Biology course instruction from knowledge transmission to cognitive cultivation, demonstrating significant improvements in students’scientific reasoning, self-regulated learning capacities, and innovative practical abilities. This teaching innovation offers a forward-looking and implementable pathway for reforming core STEM curricula in the modern era.
  • LI Ting-Ting, LU Ping, QI Yu-Shan, GAO Chun-Yan
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 542-549. https://doi.org/10.13865/j.cnki.cjbmb.2025.12.1341
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    Ideological and political education within university courses is essential for fulfilling the institution’s core mission of cultivating virtue through education. As artificial intelligence technology increasingly penetrates the educational domain, the need to reform and innovate curriculum-based ideological and political instruction has become pressing. Generative Artificial Intelligence (Generative AI), a significant subset of AI, presents new avenues for overcoming teaching challenges and transforming educational methodologies through its extensive database and advanced interactive understanding and dialogue capabilities. This study investigates the application of Generative AI in the ideological and political education of the course “Clinical Immunological Testing Techniques,” aiming to improve the efficacy of moral education in teaching and to achieve a seamless integration of knowledge transfer, skill development, and value guidance. Utilizing Generative AI technology, we intelligently extracted and reconstructed ideological and political content from the curriculum, creating a human-AI collaborative teaching model structured around “precise pre-class preparation—collaborative in-class inquiry—post-class reflection and internalization”. Students from the Class of 2021 (n=219) and Class of 2022 (n=217) in the Medical Laboratory Science program were designated as the control and research groups, respectively. Teaching interventions were conducted under uniform conditions, including the same teaching teams, course content, and assessment criteria. The effectiveness was evaluated by comparing the two groups across various metrics: academic performance in professional knowledge, practical skills, learning behavior data (encompassing classroom participation and AI interaction frequency), and questionnaire responses. Results indicated that the research group significantly outperformed the control group in professional knowledge and practical skills (P<0.001). Learning behavior data revealed higher AI interaction frequency and discussion participation rates in the research group. Moreover, 89.2% of students expressed a positive attitude towards AI-enhanced ideological and political education. In conclusion, the implementation of Generative AI in “Clinical Immunological Testing Techniques” has contributed to enhancing students’ professional competence and practical abilities, enabling the precise integration of ideological elements, and facilitating the subtle infusion of value guidance, thus providing a reproducible and practical model for the reform of ideological and political education in medical courses.
  • JI Lin-Dan, JIN Xiao-Feng, XU Jin, CAI Jie, LI Hai-Bo, YAN Lu-Lu
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 550-558. https://doi.org/10.13865/j.cnki.cjbmb.2026.01.1452
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    Driven by the new wave of technological revolution, big data, artificial intelligence (AI), and genetic technologies are profoundly integrating into the medical field, systematically transforming healthcare models and practices. As a reconstruction of the medical education system and philosophy, the “New Medical Education” (NME) initiative responds to demands of technological advancement and educational transformation. Grounded in the fundamental mission of fostering virtue through education, the curriculum team systematically explores a digital intelligence-integrated curriculum reform pathway for Medical Genetics to overcome traditional teaching limitations, including spatiotemporal constraints, insufficiently digital-intellectualized resources, and personalized teaching challenges. This is achieved through upgrading teaching resources via a “Basic-Clinical” integrated massive open online courses (MOOC), a virtual simulation experiment platform for tiered professional training, deep integration of curriculum-based ideological and political education resources, and advanced scientific research modules; constructing a smart curriculum system by integrating knowledge-problem-competency maps with AI learning companions; and designing flexibly configurable teaching plans for diverse learner needs. Empirical results demonstrate that the reform significantly enhances teaching quality and student competency, establishing an intelligent teaching model characterized by “medical-education synergy, science-education integration, and virtual-real combination.” This provides a replicable paradigm for the digital transformation of medical education, thus contributing to cultivating high-quality innovative medical talents equipped for the intelligent era.
  • XU Hong-Xiang, LI Pei-Bo, XIE Jian-Ping
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 559-565. https://doi.org/10.13865/j.cnki.cjbmb.2026.02.1422
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    Tuberculosis (TB) remains a major global public health threat, and the worsening of multidrug-resistant tuberculosis has further intensified the challenges in its prevention and control. Conventional diagnostic methods are limited by their low sensitivity and significant delays, while the introduction of artificial intelligence (AI) technology offers a breakthrough solution for TB control. In terms of diagnosis, AI technologies significantly improve the efficiency of TB screening and enable accurate identification of disease manifestations. Meanwhile, AI also plays an important role in the discovery of TB biomarkers, where it identifies high-performance novel diagnostic markers through the analysis of multi-omics data. In the field of treatment, AI models can predict drug efficacy and the risk of adverse reactions, supporting personalized therapeutic strategies. In drug development, AI accelerates the discovery of drug targets and the screening of compounds for tuberculosis, and even enables the de novo design of novel drugs. This review summarizes the latest applications of AI in the diagnosis, treatment, and drug development of tuberculosis, aiming to clarify the current role of AI in TB control and outline future research directions.
  • Reviews
  • DENG Qian-Hui, FU Yu, LIU Chun-Hua
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 566-575. https://doi.org/10.13865/j.cnki.cjbmb.2025.12.1265
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    Atherosclerosis (AS) is a vascular disease characterized by lipid deposition, chronic inflammation, and plaque formation, serving as the primary pathological basis for cardiovascular events. Although conventional lipid-lowering therapies have achieved certain clinical efficacy, the underlying core pathogenesis remains to be further elucidated. In recent years, the gut-brain axis, a bidirectional regulatory network connecting the gastrointestinal tract and central nervous system, has gradually become a research hotspot in AS due to its pivotal role in the interaction between neuroendocrine immunity and metabolism. The gut-brain axis influences AS progression through the gut microbiota-derived metabolites such as short chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO) and intestinal hormones, which modulate host inflammation, lipid metabolism, and endothelial function; the autonomic nervous system (sympathetic/parasympathetic) affects plaque stability by regulating immune cell activity and inflammatory cytokine release. Dysregulated neuro-metabolic crosstalk may exacerbate microbial imbalance and metabolic disturbances, promoting a vicious cycle of AS progression. This review systematically summarizes the complex bidirectional signaling mechanisms between gut microbiota and the host nervous system, as well as their roles in the pathogenesis and progression of AS. It explores how gut microbiota regulate the host’s neuroendocrine and immune responses through metabolic products, thereby influencing the function of both the central and peripheral nervous systems; conversely, neural activities can also directly or indirectly modulate the homeostasis of the gut microbiota. Finally, the paper further outlines interventional strategies targeting the gut-brain axis for the treatment of AS and discusses their clinical feasibility. These findings provide theoretical foundations for developing precision prevention and treatment strategies centered on gut-brain axis regulation, while also identifying promising new targets and research directions for clinical interventions.
  • LI Wei-Yan, JIN Xiao-Feng, YE Meng
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 576-591. https://doi.org/10.13865/j.cnki.cjbmb.2025.12.1322
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    Endometrial carcinoma (EC) is one of the most common malignancies of the female reproductive system, and its incidence continues to rise. While diagnostic and therapeutic approaches have advanced, the prognosis for patients with advanced-stage remains poor. Emerging treatment strategies, particularly targeted therapies, offer new hope and underscore the urgent need for novel therapeutic targets. The ubiquitin-proteasome system (UPS), a key pathway for intracellular protein degradation, significantly influences cancer progression by regulating key proteins in oncogenic pathways through ubiquitination or deubiquitination. microRNAs (miRNAs) are a class of small RNAs widely present in eukaryotic cells that regulate gene expression and the cell cycle by binding to specific mRNAs and inhibiting their posttranscriptional expression. They can also directly target key ubiquitin ligases or deubiquitinating enzymes (DUBs), affecting downstream pathways. This review discusses how ubiquitin ligases or deubiquitinating enzymes regulate related proteins in several signaling pathways in EC and explores the mechanisms by which abnormally expressed microRNAs influence oncogenesis by targeting mRNAs of proteins in the UPS. By elucidating the roles of dysregulated ubiquitination and deubiquitination from RNA and protein perspectives, this study identifies potential therapeutic strategies and provides new insights into molecular diagnostic markers and treatments for EC.
  • LI Ming-Yue, CHEN Ming-Xing, ZOU Wei
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 592-603. https://doi.org/10.13865/j.cnki.cjbmb.2026.03.1629
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    Intracerebral hemorrhage (ICH) is a subtype of hemorrhagic stroke with extremely high mortality and disability rates, caused by the spontaneous rupture of non-traumatic cerebral blood vessels and the subsequent infiltration of blood into brain tissue. Due to its high incidence and poor long-term prognosis, it imposes a heavy burden on patients’ lives and the economy. Therefore, minimizing the neurological deficits after injury has become an urgent problem to be solved. In recent years, the role of extracellular vesicles (EVs) in mediating complex intercellular signaling and maintaining brain tissue homeostasis has attracted attention. Most EVs have good biocompatibility, stable membrane structure, low immunogenicity, and the ability to carry various bioactive molecules, providing favorable conditions for their successful passage through the blood-brain barrier and targeted regulation of brain cells. This article systematically reviews the biological and functional characteristics of EVs, thoroughly analyzes their dual regulatory roles in the pathophysiological process of cerebral hemorrhage, interprets the application potential of EVs as biomarkers for dynamic disease monitoring in the diagnosis of cerebral hemorrhage, and highlights the latest progress and improvement strategies of EVs as drug delivery and gene editing vehicles. This review aims to provide theoretical support for the precise clinical application of EVs in the diagnosis and treatment of cerebral hemorrhage.
  • LI Zhuo-Yue, FAN Hua, ZENG Wen-Xian
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 604-615. https://doi.org/10.13865/j.cnki.cjbmb.2026.03.1625
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    Mitochondria are the energy centers of cells, and their gene expression regulation is essential for maintaining cellular homeostasis. The mitochondrial genome is a circular double-stranded DNA molecule, and its transcription depends on a transcriptional machinery composed of multiple nuclear-encoded proteins. During transcription initiation, POLRMT uses NAD as a non-canonical initiation nucleotide at the start of transcription, forming a 5′NAD cap, which links transcription with the cell′s metabolic state. The mitochondrial DNA is transcribed into long, continuous polycistronic precursor transcripts, which require subsequent processing and modification to become mature. These steps take place in mitochondrial RNA granules, where they regulate RNA stability and translation efficiency. Once matured, RNA not only stays in the mitochondrial matrix but can also be transported to the cytoplasm and nucleus. This review summarizes recent advances in mitochondrial DNA transcription and post-transcriptional processing and modification, with an emphasis on the underlying mechanisms and their sub-mitochondrial localization. It further focuses on the roles of mitochondrial RNA modifications in regulating RNA stability, translation efficiency, and gene expression, and discusses the distribution and transport mechanisms of mature mitochondrial RNA. This review aims to clarify the regulatory mechanisms of mitochondrial gene expression and to provide new insights into the mechanisms underlying mitochondrial dysfunction-related diseases and potential therapeutic targets.
  • YAO Bo, HUANG Jing-Ting, HAN Ya-Guang
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 616-627. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1367
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    Polycystic ovary syndrome (PCOS) is one of the most prevalent endocrine, metabolic, and reproductive disorders among women of reproductive age, with increasing incidence worldwide, posing significant threats to female reproductive health and long-term quality of life. The syndrome is clinically characterized by hyperandrogenemia (HA), ovulatory dysfunction, and polycystic ovarian morphology, and is frequently accompanied by insulin resistance (IR), dyslipidemia, and a chronic low grade inflammatory state. In recent years, with advances in molecular research, ferroptosis, a novel form of iron-dependent regulated cell death, has been implicated as a key player in the pathogenesis of PCOS. Multiple types of non-coding RNA (ncRNA), including microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA), have been shown to finely regulate ferroptosis through various mechanisms targeting iron metabolism, redox homeostasis, lipid metabolism, and related signaling pathways. This ncRNA-mediated regulatory network of ferroptosis is extensively involved in core pathological processes of PCOS, such as granulosa cell (GC) dysfunction, follicular development arrest, excessive androgen synthesis, and dysregulated insulin secretion, thereby contributing to disease progression at multiple levels. This review systematically summarizes the core molecular mechanisms of ferroptosis, highlights the specific roles of ncRNAs in modulating ferroptosis, and elaborates on the potential implications of this regulatory axis in PCOS and its related complications. Furthermore, current limitations and challenges in studying ncRNA-regulated ferroptosis in PCOS are discussed, along with prospective directions for future research. This review aims to provide new theoretical insights into the molecular pathology of PCOS and to offer potential strategies for ncRNA-based clinical diagnosis and therapeutic interventions.
  • FAN Min-Min, SHEN Liang-Liang
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 628-641. https://doi.org/10.13865/j.cnki.cjbmb.2026.02.1317
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    Dysregulation of cholesterol homeostasis plays a pivotal role in tumorigenesis, progression, and immune evasion. This review summarizes the core regulatory mechanisms of intracellular cholesterol metabolism, including biosynthesis mediated by sterol regulatory element-binding protein 2 (SREBP2) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), low-density lipoprotein receptor (LDLR)-dependent exogenous uptake, ATP-binding cassette transporter A1/G1 (ABCA1/ABCG1)-driven efflux, and esterification catalyzed by acyl-CoA:cholesterol acyltransferase 1/2 (ACAT1/2). It further systematically elaborates on the multidimensional regulatory functions of these metabolic pathways within the tumor immune microenvironment (TIME). In the TIME, tumor cells reprogram their own and surrounding immune cells’ cholesterol metabolism to establish an immunosuppressive milieu. Specifically, enhanced ACAT1 activity leads to cholesterol ester accumulation in T cells, impairing receptor clustering and effector function. Oxysterols, such as 25-hydroxycholesterol (25-HC) and 27-hydroxycholesterol (27-HC), modulate macrophage polarization, inhibit dendritic cell (DC) migration, and induce T cell exhaustion via liver X receptor (LXR) signaling. The functional maturation of myeloid-derived suppressor cells (MDSCs) is also regulated by the XBP1-cholesterol axis. Moreover, the antitumor activity of natural killer (NK) cells is negatively regulated by LDLR-mediated cholesterol uptake and the bile acid metabolite iso-lithocholic acid (iso-LCA). Targeting cholesterol metabolism demonstrates significant antitumor potential: statins inhibit the mevalonate pathway; inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9) or niemann-pick C1-like 1 (NPC1L1) block cholesterol uptake; and the ACAT inhibitor avasimibe not only directly suppresses tumor growth but also reverses immunosuppressive states. Notably, combining cholesterol metabolism modulators with immune checkpoint inhibitors produces synergistic effects, significantly enhancing antitumor immunity. Therefore, cholesterol metabolism serves not only as a metabolic foundation for tumor cell proliferation but also as a critical metabolic hub regulating TIME function. Its precise intervention holds promise for developing novel and effective combinatorial strategies for cancer therapy.
  • ZHOU Yi, LI Zhao-Kun, LIANG Nan
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 642-652. https://doi.org/10.13865/j.cnki.cjbmb.2025.12.1242
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    Protein kinase C substrate 80K-H, also known as the Glucosidase Ⅱ beta subunit, interacts with the Glucosidase Ⅱ alpha subunit to jointly participate in regulating the processing and maturation of glycoproteins in the endoplasmic reticulum, and plays an important role in N-glycosylation, a key post-translational modification. At present, the close relationship between PRKCSH gene mutations and Autosomal Dominant Polycystic Liver Disease has been widely studied and concerned. The multiple functions of PRKCSH, including regulating signaling pathways such as IGF1R and IRE1α, make it a promising therapeutic target and biomarker for cancer immunotherapy. Meanwhile, in cancer, PRKCSH can affect cell growth, metastasis, and responses to growth factors through pathways such as responding to endoplasmic reticulum stress, coordinating cell death programs, and participating in immunotherapy, thereby influencing autophagy or apoptosis. PRKCSH can also enhance cancer treatment and regulate anti-tumor immunity by boosting the activity of NK cells and T cells. In addition, PRKCSH can generate different isoforms through alternative splicing, affecting processes such as epithelial-mesenchymal transition and lung cancer cell proliferation. Although PRKCSH has been identified in various diseases, more evidence is still needed to clarify its specific mechanism of action and development potential.
  • Research Papers
  • ZHAO Hai-Hong, HE Xin-Yu, LI Wei-Xin, LI Xue-Mei, ZHANG Yu-Qi, DU Lei, DONG Cheng-Guang, LI Cheng-Qi
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 653-666. https://doi.org/10.13865/j.cnki.cjbmb.2026.03.1319
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    Fiber quality is an important economic trait of cotton and one of the major breeding targets. In this study, 408 upland cotton accessions were genotyped using the CottonSNP80K chip, yielding 12 874 high-quality SNP linkage disequilibrium block (SNPLDB) markers. A total of 128 SNPLDBs significantly associated with fiber length, 163 with fiber strength, 149 with fiber fineness, 94 with fiber uniformity, and 92 with fiber elongation were detected across six environments (five single environments and one multi-environment) using restricted two-stage multi-locus genome-wide association analysis (RTM-GWAS). Among these, 10, 13, 9, 4 and 4 SNPLDBs associated with the five traits, respectively, were detected in at least two environments. Further single-marker/haplotype analysis revealed significant phenotypic differences among alleles of 6, 12, 9, 3 and 3 SNPLDBs associated with these five traits, respectively. A total of 11 loci associated with fiber length, 15 with fiber strength, 8 with fiber fineness, 6 with fiber uniformity, and 4 with fiber elongation identified in this study were found to overlap with QTLs/markers reported in previous studies. Among them, the loci Block_A13_74977977_75077975 (associated with fiber strength), Block_A05_24309961_24322003 and Block_D03_2459185_2528302 (associated with fiber fineness), and Block_D04_47711028_47718399 (associated with fiber elongation) were detected in multiple environments in this study as well as in previous studies. Combining GO enrichment and RNA-seq analysis indicated that 8 genes related to fiber length, 5 genes related to fiber strength, 8 genes related to fiber fineness, 4 genes related to fiber uniformity, and 3 genes related to fiber elongation may be potential candidate genes for fiber quality. This study provides a new perspective for elucidating the genetic basis of fiber quality in upland cotton and lays an important foundation for molecular breeding of fiber quality.
  • WANG Sa-Ri-Na, TONG He, WANG Li
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 667-677. https://doi.org/10.13865/j.cnki.cjbmb.2026.03.1433
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    Protein arginine methyltransferase 1 (PRMT1), a key enzyme regulating protein arginine methylation, is involved in the development of various tumors. This study aimed to investigate the role of PRMT1 in hepatocellular carcinoma (HCC) progression and its clinical significance. We first analyzed the pan-cancer expression patterns of PRMT1 and its association with prognosis by integrating public databases such as TCGA, GTEx, and GEPIA2. Subsequently, real-time quantitative PCR (qPCR) and Western blotting were used to detect PRMT1 expression in the HCC cell line Huh7, and its subcellular localization was determined by immunofluorescence. Transwell and wound healing assays were further employed to assess the effect of PRMT1 knockdown on the migration and invasion abilities of Huh7 cells. Integrated analysis of public databases including TCGA revealed that PRMT1 expression was significantly upregulated in multiple tumor tissues (P < 0.05), and its high expression was associated with poor patient prognosis. Functional enrichment analysis indicated that PRMT1 is mainly involved in pathways such as the cell cycle and DNA repair. In cellular experiments, qPCR and Western blotting results showed that PRMT1 was highly expressed in the HCC cell line Huh7. Immunofluorescence further confirmed that PRMT1 was primarily localized in the nucleus. Transwell and wound healing assays demonstrated that knockdown of PRMT1 significantly reduced the migration and invasion abilities of Huh7 cells. These findings indicate that PRMT1 exhibits high expression and nuclear localization in HCC and regulates the migration and invasion processes of HCC cells, providing new experimental evidence for understanding the role of PRMT1 in the development and progression of HCC.
  • QIAN Song, ZHU Si-Qi, QI Xin, JIANG Ling-Xia, XIE Song-Xu, CHEN Chao-Yue, WANG Bin-Jie
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 678-687. https://doi.org/10.13865/j.cnki.cjbmb.2026.03.1651
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    Methcathinone, a widely abused synthetic cathinone, poses a significant public health risk because of its severe neurotoxicity and high addictive potential. In this study, we used a zebrafish model to investigate the mechanisms underlying its neurobehavioural effects. Methcathinone exposure reduced larval survival and induced a range of abnormal behaviours. Most notably, conditioned place preference (CPP) tests demonstrated the potent rewarding properties of methcathinone, as shown by a significant 22.2% increase in time spent in the drug-paired light zone compared with baseline(P<0.01). Transcriptomic analysis of brain tissue revealed systemic disruption of the neuroactive ligand-receptor interaction pathway. Gene set enrichment analysis (GSEA) further revealed significant suppression of γ-aminobutyric acid (GABA) signalling (NES =-1.64, P<0.05) and glutamate receptor signalling, including ionotropic and AMPA receptor signalling (P<0.05). Quantitative PCR validation confirmed the marked downregulation of key genes involved in these pathways: the mRNA expression of GABAergic receptors(e.g., gabra1 and gabra2), glutamatergic receptors (e.g., gria2 and grin2B), and the dopamine transporter slc6a3 decreased by 67.0% to 97.9% (all P <0.01). These results suggest that methcathinone drives reward-seeking behaviour through a synergistic dual-target mechanism; specifically, the concurrent suppression of GABAergic inhibition and slc6a3-mediated reuptake likely facilitates dopaminergic hyperactivity, whereas the downregulation of glutamate receptors reflects a homeostatic response to overstimulation. Our findings provide novel mechanistic insight into the development of methcathinone use disorder in humans.
  • XU Jing, LIU Sen-Yang, WANG Xu-Feng, SUI Hui-Xin, ZHANG Chun-Jing, SUN Zhao-Jie, CHENG Hao, QI Xiao-Dan
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 688-696. https://doi.org/10.13865/j.cnki.cjbmb.2026.03.1635
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    Exendin-4 (Exe), a glucagon-like peptide-1 (GLP-1) receptor agonist, has a protective effect on pancreatic β cells; however, its underlying mechanism is not well understood. In this study, Exendin-4 exhibited a higher antioxidant ability and protected MIN6 cells from high glucose-induced oxidative damage by reducing reactive oxygen species (ROS) production (P < 0.01), and maintaining mitochondrial function in pancreatic β cells. The beneficial effects of Exendin-4 included increased cell viability (P < 0.05) and insulin secretion (P < 0.05), as well as improved mitochondrial membrane potential (MMP) (P < 0.01) and ATP levels (P < 0.05). Additionally, Exendin-4 inhibited lactate dehydrogenase (LDH) activity (P < 0.001) and reduced intracellular malondialdehyde (MDA) levels (P < 0.01), and boosted the activities of antioxidant enzymes such as superoxide dismutase (SOD) (P < 0.01) and catalase (CAT) (P < 0.01). Glutaredoxins (Grxs) were identified as glutathione (GSH)-dependent oxidoreductases, and the Grx/GSH system is commonly referred to as the cellular antioxidant system acting in the defense of pancreatic β cells against oxidative stress and the mitochondrial damage. Our findings revealed that Exendin-4 significantly enhanced the protein expression levels of glutaredoxin 1 (Grx1), glutaredoxin 2 (Grx2) and glutathione reductase (GR) (P < 0.05), and improved the GSH/GSSG ratio (P < 0.01) and NADPH/NADP+ ratio (P < 0.05). These results indicate that Exendin-4 improved the function of pancreatic cells under high glucose condition. The underlying mechanism involves increasing the expression levels of key proteins in the glutaredoxin system and inhibiting the dysfunction of the Grx/GSH system, thereby reducing mitochondrial oxidative damage and functional disorders.
  • Techniques and Methods
  • YE Xue-Fei, XIE Ai-Nan, ZHOU Xiao-Shuang, CHEN Kang-Mei, LIU Ming-Dong
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 697-707. https://doi.org/10.13865/j.cnki.cjbmb.2026.03.1518
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    Plasmids are fundamental tools in the life sciences and biomedical research; however, developing efficient and low-cost extraction methods remains a major challenge. Here, we evaluated silica particles of diverse morphologies and sizes as DNA adsorbents, optimized the alkaline lysis buffer, and systematically refined critical parameters, including chaotropic salt concentration, silica dosage, and adsorption and elution kinetics. These optimizations substantially improved extraction performance. The resulting protocol is streamlined, inexpensive, and consistently yields high-quality plasmid DNA, with outputs comparable to those obtained using commercial spin-column kits. Moreover, the method is linearly scalable, achieving yields and purity similar to those of silica membrane-based Maxiprep columns, and is fully compatible with downstream applications such as restriction digestion and cell transfection. Collectively, this work provides a robust and scalable plasmid extraction strategy with strong potential for commercial translation.
  • Education and Teaching
  • LV Hong-Ming, ZHENG Yu-Wei, YAN Ke-Xin, LIU Yang, ZHANG Jie-Xing, GE Yan-Song, BAI Yun-Long, ZHENG Jia-San
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 708-714. https://doi.org/10.13865/j.cnki.cjbmb.2025.12.1370
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    Animal Biochemistry is a core foundational course in animal husbandry and veterinary majors at agricultural universities, serving as a cornerstone for cultivating molecular experimental skills at the graduate level. The current New Agriculture Education initiative explicitly calls for “cultivating agricultural talents with profound disciplinary knowledge”. However, the traditional Animal Biochemistry curriculum system can no longer adequately meet this objective, making the promotion of innovative practices in this course an inevitable choice for agricultural education reform. This study adopts the “Integration of Knowledge and Practice” teaching innovation method and the BOPPPS (bridge-in, objective, pre-assessment, participatory learning, post-assessment, and summary) instructional model, leveraging the Small Private Online Course (SPOC) interactive learning platform to integrate online and offline, in-class and extracurricular teaching resources. The reform is advanced in three key aspects: first, restructuring the teaching content to strengthen the connection between knowledge and practice; second, incorporating ideological and political elements into the curriculum to achieve value guidance; and third, improving a diversified evaluation system to comprehensively assess learning outcomes. Through these measures, the course has successfully transitioned from a “traditional knowledge-transmission classroom” to an “ability-oriented, innovation-driven, open and integrated classroom,” achieving the three-dimensional teaching goals of “knowledge impartation, ability cultivation, and value shaping”. This effectively nurtures new-era agricultural talents with the qualities of “understanding agriculture, loving agriculture, strengthening agriculture, and revitalizing agriculture”, thereby providing crucial talent support for the modernization of China’s agricultural development.
  • Cover Image Introduction
  • Cover picture designer YANG Yi-xuan, Morigen
    Chinese Journal of Biochemistry and Molecular Biology. 2026, 42(4): 715-715.
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