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    CJBMB: 40 Years of Biochemistry and Molecular Biology in China Advances in Basic and Clinical Research of Rhabdomyosarcoma
  • The Past, Present, and Future of Rhabdomyosarcoma
    ZANG Ming-Xi
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1737-1739. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1366
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    Rhabdomyosarcoma, the most common soft tissue sarcoma in children, poses significant research challenges due to its diverse subtypes, anatomical locations, and cellular origins. While advances have been made in understanding its complex genetic landscape—including chromosomal translocations, gene mutations, and factors linked to skeletal muscle development—many questions remain unresolved. Future studies should focus on elucidating the molecular mechanisms driving the fate of rhabdomyosarcoma progression and refining its genomic profile. Such efforts will provide a critical foundation for developing personalized prevention and therapeutic strategies for rhabdomyosarcoma.
  • Epigenetic Regulation in Rhabdomyosarcoma
    LIU Shuang-Ai, CHEN Xue, TAO Ting
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1740-1751. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1303
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    Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma, characterized by high heterogeneity and strong invasiveness. The occurrence and progression of RMS involve multiple epigenetic regulatory mechanisms, including DNA methylation, histone modification, chromatin remodeling, and non-coding RNA regulation. These epigenetic alterations influence tumor initiation, maintenance, metastasis, and drug resistance by modulating gene expression and key signaling pathways. Typical epigenetic regulatory targets include the BET protein family, histone deacetylases (HDACs), and EZH2. Epigenetic drugs developed against these targets have already shown promising activity in preclinical studies and early-phase clinical trials. In addition, combination strategies are gaining increasing attention, such as the use of EZH2 or HDAC inhibitors together with chemotherapy, differentiation inducers, or immune checkpoint inhibitors, which can enhance efficacy and overcome resistance. Future research directions will rely on integrative multi-omics approaches and cutting-edge technologies to overcome the limitations of current models and datasets, thereby uncovering novel mechanisms of epigenetic regulation in RMS. By integrating precision medicine with multi-omics insights, it will be possible to identify new biomarkers and potential targets, providing a foundation for the development of personalized epigenetic therapies and ultimately improving the clinical management of pediatric RMS.
  • Rhabdomyosarcoma: Insights into Tumor Progression Through The Aspect of Differentiation
    CHEN Ye-Xi, LI Zhi-Jie
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1752-1758. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1340
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    Rhabdomyosarcoma (RMS) is one of the most common malignant soft-tissue tumors in children and adolescents, characterized by a blockade of skeletal-muscle differentiation. Here we summarize basic studies and key advances in the field. We cover three aspects in RMS: differentiation control, cell-cycle regulation, and signaling networks. During early differentiation, Myogenic Differentiation 1 (MyoD) heterodimerizes with E-proteins and initiates muscle-lineage gene programs together with muscle-specific miR-206 and selected lncRNAs. During late differentiation, Myogenin orchestrates myoblast fusion and myotube maturation, while its activity and stability are modulated by upstream regulators including the miR-1-TRPS1 axis, Arp5, and IL-4/STAT6. At the cell-cycle level, the p21/p27 and Rb-E2F axes promote G1 arrest to license differentiation. When these signaling pathways are disrupted, tumor cells maintain high proliferative activity, but cell differentiation is blocked. At the signaling level, aberrant activation of PI3K/AKT/mTOR and MAPK/ERK, together with differentiation-suppressive pathways such as Notch and Hedgehog, interconnect to form a self-sustaining “proliferation-de-differentiation” loop. Mechanistically informed strategies—including inhibition of aberrant pathways, correction of epigenetic and non-coding RNA imbalances, restoration of MyoD/Myogenin function, and CRISPR-based precision interventions—show potential to induce differentiation and restrain tumor progression. Remaining challenges include unclear causal relationships among pathways and subtype-specific drivers, a paucity of predictive biomarkers, and insufficient definition of therapeutic windows and resistance dynamics for combination regimens. Future work should leverage single-cell and spatial omics to integrate epigenetic and post-transcriptional layers, reconstruct actionable differentiation networks, and—under biomarker guidance—develop and stratify cross-pathway combination strategies to advance RMS differentiation therapy toward precision and clinical translation.
  • Epigenetic Mechanisms in Rhabdomyosarcoma
    HAN Tong, WANG Heng-Rui, ZANG Ming-Xi
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1759-1764. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1353
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    Rhabdomyosarcoma is the most common soft tissue sarcoma in children, and its primary cause lies in the impaired differentiation of skeletal muscles. The development of skeletal muscles is dynamically regulated by multiple factors, which form core regulatory circuits predominantly governed by muscle-specific enhancers. Once erroneous enhancer connections occur, they will unlock phenotypic plasticity, causing cells to deviate from their normal differentiation path and enter an abnormal proliferative state, ultimately forming rhabdomyosarcoma. This process requires the coordinated action of chromatin remodeling factors. Additionally, as a pediatric tumor, rhabdomyosarcoma has a low mutational burden. It is precisely this non-mutational epigenetic reprogramming that unlocks phenotypic plasticity in the normal skeletal muscle differentiation process, thereby leading to the development of rhabdomyosarcoma. This article summarizes the role of epigenetic regulation during the onset and progression of rhabdomyosarcoma, with a focus on analyzing DNA methylation, histone methylation, acetylation, non-coding RNAs (such as miRNA, lncRNA, circRNA, and eRNA), chromatin remodeling, and RNA modifications, aiming to lay a theoretical foundation for the prevention and treatment of rhabdomyosarcoma.
    • Hotspot Mini-Review
  • Structure and Function of Alkane Monooxygenase
    ZONG Zi-Wei, ZHAO Jing, XIAO Rong
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1765-1772. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1250
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    Every year, up to 800 million tons of hydrocarbons enter the environment globally, most of which are alkanes. Due to the inactive property and the high freezing points, alkanes have caused serious problems on environmental ecology and oil recovery. Alkane monooxygenase (AlkB) is a transmembrane metalloproteinase, and belongs to the membrane-bound fatty acid desaturase (FADS) family, which is able to convert straight-chain alkanes into the corresponding primary alcohols during the first step of alkane degradation mediated by microorganisms. Thus, AlkB plays a crucial role in the global carbon cycle and bioremediation of oil pollution. In this paper, the characteristics, structure, active site, catalytic mechanism, and the construction of recombinant bacteria of AlkB from different microorganisms were reviewed. In addition, the important significance of AlkB for environmental remediation and oil extraction was also emphasized, which would provide new clues for the bioremediation of hydrocarbon-contaminated sites and improvement of oil recovery rate by AlkB.
    • Review
  • Progress and Potential Clinical Applications of microRNA in Multiple Myeloma
    JING Hua-Qing, ZHAO Chen, HAO Mu
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1773-1780. https://doi.org/10.13865/j.cnki.cjbmb.2025.08.1033
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    Multiple myeloma (MM) is a highly heterogeneous hematologic malignancy characterized by increasing incidence rates and currently incurable nature, underscoring the urgent need for more effective treatment approaches. In recent years, significant progress has been made in microRNA (miRNA) research related to MM, providing new insights into disease pathogenesis and facilitating the development of innovative diagnostic approaches and treatment strategies. In this review, we systematically summarized the molecular mechanisms by which dysregulated miRNAs affect tumor cell functions, bone marrow microenvironment and drug resistance through the regulation of critical biological processes including cell cycle progression, metabolic reprogramming, apoptosis, differentiation, and cell migration. Meanwhile, we also highlight the promising potential of miRNAs as therapeutic targets and their clinical value in disease prognosis and diagnosis. Finally, this review discusses the risks and challenges of miRNA-based therapeutic strategies, particularly focusing on delivery efficiency and targeting specificity, while proposing potential solutions for future research directions. By comprehensively analyzing the current state of miRNA research in MM, this review aims to promote the clinical translation of miRNA-based therapies and provide valuable references for clinical practice.
  • From Bench to Bedside: Current Research Status of Mitophagy in Acute Respiratory Distress Syndrome (ARDS)
    LI Mei-Ling, XU Xi-Yuan
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1781-1788. https://doi.org/10.13865/j.cnki.cjbmb.2025.08.1177
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    Acute respiratory distress syndrome (ARDS), a clinical critical disease characterized by acute progressive respiratory failure, has a high mortality rate and poses a serious threat to human health. In the pathological process of ARDS, mitophagy is often overly activated or dysfunctional, interacting with inflammatory responses and apoptosis to exacerbate lung injury. The basic mechanisms of mitophagy include the PINK1/Parkin-mediated mitophagy pathway and the receptor-mediated mitophagy pathway. Mitophagy is related to the pathogenesis of ARDS, inflammatory response and apoptosis. Many pathogenic factors in ARDS can cause abnormal mitophagy (excessive activation or dysfunction). Excessive activation can lead to excessive consumption of mitochondria and disorder of energy metabolism, and dysfunction causes damaged mitochondria to accumulate and release pro-inflammatory factors, which aggravates lung injury. Mitophagy and inflammatory response are regulated reciprocally: inflammatory response aggravates lung injury through reactive oxygen species (ROS) and NLRP3 activation while mitophagy can remove damaged mitochondria to inhibit inflammation. On the contrary, inflammatory factors form a vicious circle by inhibiting mitophagy, and mitophagy has a dual role in apoptosis. Normally, it inhibits apoptosis by removing damaged mitochondria, while excessive activation or dysfunction promotes apoptosis due to energy exhaustion or releases of pro-apoptotic factors (such as cytochrome C, mtDNA), and synergistically aggravates lung injury with endoplasmic reticulum stress and other pathways. In addition, existing drugs that regulate mitophagy include rapamycin (RAPA), mitochondrial division inhibitor 1 (Mdivi-1) and melatonin (MT), which can regulate mitophagy and bring new directions for the treatment of ARDS. But these drugs suffer from poor specificity and side effects. Therefore, the complexity of mechanism of mitophagy brings multiple challenges to drug development. In the future, in-depth research on the mechanism of mitophagy in different stages of ARDS, the development of highly specific regulators, clinical studies, and the integration of multi-omics technologies are expected to break through the treatment bottleneck and improve patient prognosis.
  • The Role of the SNARE Complex in Dopamine Deficiency of Attention Deficit Hyperactivity Disorder (ADHD)
    ZHANG Yu-Yan, WU Chen-Lei, ZHOU Rong-Yi
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1789-1798. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1045
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    Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in children and adolescents, and is clinically characterized by inattention, hyperactivity, and impaired impulse control. Despite extensive research, its etiology and pathogenesis remain incompletely understood. The dopamine (DA) deficiency theory constitutes a central framework in current ADHD studies. In-depth investigations of dopamine transporter (DAT) and dopamine receptor (DR) functions have led to the development of mainstream pharmacological treatments, which alleviate symptoms by enhancing DA concentrations and further support the essential role of the dopaminergic system in ADHD. Beyond DA transport and receptor signaling, recent findings suggest that impaired DA release may contribute to DA deficiency. The soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex, composed of synaptosomal-associated protein 25 (SNAP-25), syntaxin-1A (STX1A), and vesicle-associated membrane protein 2 (VAMP2, also known as synaptobrevin 2), serves as the core molecular machinery mediating synaptic vesicle docking and membrane fusion at the presynaptic terminal. As the minimal apparatus driving DA vesicle exocytosis, the SNARE complex precisely regulates presynaptic DA release through coordinated vesicle fusion and recycling. Functional disruptions in SNARE complex assembly, disassembly, or its auxiliary regulatory proteins may hinder effective DA transmission, potentially contributing to DA deficiency and representing a novel molecular mechanism in ADHD pathogenesis. This review summarizes the current understanding of the SNARE complex and its regulatory network, emphasizing their potential roles in the pathogenesis and progression of ADHD, and offering theoretical insights into disease mechanisms and targeted therapeutic strategies.
    • Research Paper
  • The Effect of Folate Deficiency on Neural Spectrum Differentiation of Mouse Embryonic Stem Cells
    XIE Qi, LI Bao-Lian, ZHAO Yong-Li, LIU Zeng-Li, CAO Zhi-Hua, GU Xiao-Long, LIU Zhi-Zhen, LI Jian-Ting, YU Bao-Feng
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1799-1809. https://doi.org/10.13865/j.cnki.cjbmb.2025.10.1229
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    Mouse embryonic stem cells (mESCs) have become an ideal model for analyzing the developmental machinery of mammalian embryos due to their multidirectional differentiation potential and self-renewal properties. Folate, a core coenzyme in one-carbon metabolism, has become a global public health problem due to its deficiency in neural tube defects (NTDs), but its role in the neural pedigree differentiation of mESCs is not clear. In this study, we systematically analyzed the regulatory mechanism of folate in neural lineage differentiation and its potential association with the development of neural tube deformities based on the neural differentiation model of ESCs. Research results showed that during the differentiation of mESCs into the neural lineage, folate deficiency led to a significantly smaller diameter of embryoid bodies compared with the normal folate control group (P < 0.05). The expression level of Nestin, a neural precursor cell marker, was detected by real-time quantitative PCR (RT-qPCR) and immunofluorescence. The results showed that both the transcriptional and protein expression levels of Nestin in the folate deficiency group were decreased compared with the normal folate control group (P < 0.05). In addition, immunofluorescence staining also showed that the Ki67 fluorescence level was significantly decreased in the folate deficiency group (P < 0.05), indicating that folate deficiency impairs the proliferation ability of neural precursor cells. Meanwhile, transcriptome sequencing was performed on the key time points of neural differentiation, day 4 (D4) and day 8 (D8). The GO functional enrichment analysis of differentially expressed genes (DEGs) between the control group and the folate deficiency group at D4 and D8 respectively revealed that folate deficiency caused a bias in mesoderm differentiation, suggesting that folate deficiency may lead to abnormal neural differentiation by disrupting the balance of germ layer fate determination. The KEGG pathway analysis of DEGs between the control group and the folate deficiency group at D4 and D8 further revealed that the PI3K-AKT, MAPK and Wnt signaling pathways were significantly enriched in the folate deficiency group. Western blotting showed that the protein levels of PI3K, AKT and their phosphorylated forms in the folate deficiency group were significantly increased at D8. The use of PI3K inhibitors could significantly increase the expression levels of Nestin, Pax6 and Otx2 in the folate deficiency group (P < 0.05), thus reversing the impairment of ectoderm differentiation caused by folate deficiency. In this study, we constructed a model of the dynamics of ESC differentiation due to folate deficiency to reveal the role of folate in the process of induced differentiation of neural progenitors, which may be one of the mechanisms by which folate deficiency leads to the development of NTDs. Our study provides new perspectives for elucidating the pathogenic mechanism of neural tube malformations caused by folate deficiency, as well as a new theoretical basis for the pathogenic mechanism of similar developmental defects.
  • Interaction Between RRM2 and HIF-1α/iNOS/VEGF Signaling Pathway in Ferroptosis in Hepatocellular Carcinoma Cells and the Therapeutic Potential of Sorafenib
    LIU Hong-Chen, ZHAO Hong-Yu, XIE Tian-Hang, LIANG Chang-Min, GE Tang-Dong, LI Jing, ZHANG Peng-Xia, PIAO Jin-Hua
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1810-1822. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1160
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    Ribonucleotide reductase regulatory subunit M2 (RRM2), a key cell cycle regulatory gene, has been implicated in inducing cellular senescence, cell cycle arrest, or cell death across various cancers. Although previous studies have demonstrated the significant role of RRM2 in cancer cells, the specific mechanism by which RRM2 modulates ferroptosis via sorafenib (sorafenib, Sor) remains inadequately elucidated. This study aimed to investigate the mechanism underlying RRM2-mediated, sorafenib-induced ferroptosis in hepatocellular carcinoma (HCC) cells. Different concentrations of sorafenib (0, 10, 15, 20, 25, 30 μmol/L) were used to treat human hepatoblastoma cells (HepG2) and human hepatobiliary carcinoma cells (Huh7), and then the inhibitory effect of sorafenib on the proliferation of HepG2 cells and Huh7 cells was detected by CCK8 method. The optimal concentration for establishing HepG2 and Huh7 cell models was determined, including SOR group (transfected with empty plasmid combined with 11 μmol/L sorafenib intervention cells), OE-RRM2 group (RRM2 in overexpressed cells), OE-RRM2 sor group (transfected with RRM2 overexpression vector combined with 11 μmol/L sorafenib intervention cells), SINC group (transfected with empty vector as knockdown control), and SIRRM2-1, SIRRM2-2, and SIRRM2-3 group (RRM2 in knockdown cells). CCK-8 and plate cloning assay results indicated that RRM2 knockdown led to reduced cell proliferation, while RRM2 overexpression had the opposite effect (P＜0.05); Glutathione (GSH) assay results showed that RRM2 knockdown led to reduced cellular GSH levels, while RRM2 overexpression had the opposite effect (P＜0.05); Intracellular reactive oxygen species (ROS) assay results showed that RRM2 knockdown led to increased cellular ROS levels, while RRM2 overexpression had the opposite effect (P＜0.05); Mitochondrial membrane potential (MMP) assay results showed that RRM2 knockdown led to increased cellular MMP, while RRM2 overexpression had the opposite effect (P＜0.05); qRT-PCR and Western blot experiments showed that knocking down RRM2 led to decreased expression levels of glutathione peroxidase 4 (GPX4), glutathione synthetase (GSS), and hypoxia-inducible factor-1α (HIF-1α)/inducible nitric oxide synthase (iNOS)/vascular endothelial growth factor (VEGF) gene expression levels, while the RRM2 overexpression group showed the opposite results (P＜0.05). Immunofluorescence (IF) experiments showed that RRM2 knockdown led to a decrease of HIF-1α protein expression levels (P＜0.05). In summary, these findings suggest that sorafenib may activate RRM2 in liver cancer cells, thereby inhibiting ferroptosis. Furthermore, RRM2 may promote the malignant progression of HCC by activating the HIF-1α/iNOS/VEGF signaling pathway to suppress ferroptosis.
  • Dapagliflozin Promotes Mitochondrial Biogenesis and Induces “Browning” of White Adipose Tissue Via an AMPK-Dependent Mechanism
    WANG Wen-Di, LV Yue, LI Pei-Yang, TIAN Si-Si, HAO Jing-Nuo
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1823-1832. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1180
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    The global epidemic of obesity and related metabolic diseases represents a major public health challenge, highlighting an urgent need for effective intervention strategies. Browning of white adipose tissue (WAT) and mitochondrial biogenesis have emerged as promising therapeutic targets for improving energy metabolism; however, their regulatory mechanisms remain incompletely understood. Dapagliflozin (DAPA), a sodium-glucose cotransporter 2 (SGLT2) inhibitor, is known for its glucose-lowering effects, but whether it also exerts anti-obesity benefits by modulating adipocyte metabolism is still unclear. This study aimed to investigate whether DAPA ameliorates obesity and related metabolic disorders by promoting mitochondrial biogenesis and inducing WAT browning through an AMP-activated protein kinase (AMPK)-dependent mechanism. High-fat diet-induced obese C57BL/6J mouse models and 3T3-L1 adipocyte models were established to evaluate the interventional effects of DAPA both in vivo and in vitro. The results showed that DAPA significantly reduced the body weight, adipose tissue weight, and liver weight in obese mice (all P < 0.05), improved dyslipidemia and liver function impairment (all P < 0.05), and alleviated adipocyte hypertrophy and hepatic steatosis. Western blot and immunohistochemical analyses demonstrated that DAPA up-regulated the protein expression of uncoupling protein 1, mitochondrial transcription factor A, nuclear respiratory factor 1, peroxisome proliferator-activated receptor gamma coactivator 1-α, and phosphorylated AMPK in three types of adipose tissue, and also increased the mtDNA content (all P < 0.01). Cellular experiments further confirmed that DAPA reduced lipid accumulation in a dose-dependent manner, enhanced mitochondrial membrane potential and adenosine triphosphate levels, and promoted the expression of the above factors (all P < 0.01). These effects were partially reversed by co-treatment with the AMPK inhibitor Compound C or the mitochondrial respiratory chain inhibitor rotenone (all P < 0.01). In conclusion, our findings suggest that DAPA promotes mitochondrial biogenesis, induces WAT browning, and enhances brown adipose tissue function by activating an AMPK-dependent mechanism, thereby improving obesity and metabolic disorders. These results not only deepen the understanding of the pleiotropic effects of SGLT2 inhibitors but also provide a theoretical and experimental basis for expanding their application to the treatment of non-diabetic obesity.
  • The Role of MC4R in The PVN in Amylin-mediated Anorexia
    TIAN Dong-Hai, LI Peng-Hui, DU Chen-Guang, ZHANG Xiao-Yu
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1833-1841. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.139
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    This study aimed to investigate whether amylin regulates appetite and blood glucose through MC4R neurons in the paraventricular nucleus (PVN). To this end, we verified the appetite-suppressing effect of amylin and its activation of c-Fos in the PVN using antibody labeling and Western blot analysis. Treatment with the amylin receptor antagonist AC187 abrogated this appetite suppression and c-Fos expression in the PVN (P<0.01), indicating that amylin’s effects are primarily mediated by receptor activation. Subsequently, conditional knockout (CKO) of MC4R in the PVN was achieved by stereotaxic intracranial injection of the AAV-Cre-EGFP virus. Results showed an approximately 80% decrease in MC4R expression (P<0.01). After amylin injection, CKO mice exhibited food intake similar to that of the controls, suggesting that MC4R neurons play a partial role in appetite suppression. A glucose tolerance test further demonstrated that amylin pretreatment for 30 minutes significantly improved glucose tolerance in mice (P < 0.01), while the hypoglycemic effect of amylin was partially attenuated in CKO mice (P < 0.05), indicating that MC4R also participates in glucose regulation. To identify the types of MC4R neurons within the PVN, we used FISH and immunofluorescence to examine their co-expression with the intracellular vesicular GABA transporter (VGAT) and vesicular glutamate transporter 2 (VGLUT2). We found that MC4R primarily colocalized with VGlut2-positive excitatory neurons (≈50%, P<0.01). These results suggest that amylin can regulate appetite and glucose metabolism, in part, through MC4R excitatory neurons within the PVN, suggesting amylin’s multiple regulatory roles in energy homeostasis.
  • Recombinant Expression and Purification of Human m6A Methyltransferase METTL3 and Preliminary Functional Analysis in Lung Epithelial Cells
    LI Meng-Yu, WANG Yu-Fei, FENG Xin-Lin, JIN Ai, ZHAO Hai-Feng
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1842-1849. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1254
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    N6-methyladenosine (m6A) is the prevalent abundant internal modification in eukaryotic mRNA and plays essential roles in regulating gene expression, cell proliferation, and differentiation. METTL3, a key m6A methyltransferase, is central to this modification, yet its structural features and functional roles in cellular processes remain to be fully elucidated. This study aimed to construct a prokaryotic expression system for human METTL3 and to explore the function of its recombinant protein in lung epithelial cells. The coding sequence (CDS) of METTL3 was amplified from total RNA extracted from HEK-293T cells and cloned into the pET28a vector to generate a His-tagged fusion construct. Following IPTG induction, METTL3 was predominantly expressed in inclusion bodies. High-purity recombinant protein was successfully obtained through lysis with 8mol/L urea and purification with 200mmol/L imidazole. Western blotting confirmed the accuracy and purity of the purified His-METTL3 protein. Functional analysis revealed that treatment of BEAS-2B lung epithelial cells with recombinant METTL3 significantly promoted cell proliferation, despite no substantial change in global m6A levels. In summary, this study successfully expressed and purified functional His-METTL3 protein, and preliminarily revealed its potential role in promoting lung epithelial cell proliferation through an m6A-independent mechanism. These findings provide an experimental basis for future research into the epigenetic functions and biomedical applications of METTL3.
  • Cloning, Expression, and Characterization of the Glycosyltransferase Gene AaUGT2 from Anemarrhena asphodeloides
    CHEN Yu-Tong, ZHANG Qian, CHEN Jing, WANG Xiao-Yun, HUANG Jia
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1850-1859. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1225
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    Anemarrhena asphodeloides Bunge is one of the famous traditional Chinese medicinal herbs in China. Its extensive medicinal effects are closely related to its active ingredients. Flavonoid glycosides, as one of important active components of Anemarrhena asphodeloides, possess various pharmacological activities and have received attention from researchers in recent years. As a key downstream modification enzyme that catalyzes the production of flavonoid glycosides, glycosyltransferase plays a vital role in the biosynthetic pathway of flavonoid glycosides. However, there are few reports on flavonoid glycosyltransferases in Anemarrhena asphodeloides. Here we studied it in detail. Sequence analysis indicated that the open reading frame of AaUGT2 was 1 347 bp, encoding 448 amino acids. Real-time quantitative PCR results showed that AaUGT2 was expressed in the fibrous roots, rhizomes and leaves of Anemarrhena asphodeloides, among which the expression level of AaUGT2 was the highest in the rhizomes. Prokaryotic expression indicated that the target soluble protein of AaUGT2 was successfully expressed, and its theoretical value of recombinant protein size was 70.88 kD. In vitro enzymatic reaction experiments showed that AaUGT2 had flavonoid 7-O-glycosylation activity. In this study, the AaUGT2 gene was successfully cloned from Anemarrhena asphodeloides. We demonstrate that AaUGT2 belonged to flavonoid 7-O-glycosyltransferase, which would lay a foundation for further analysis of the flavonoid glycoside biosynthesis pathway of Anemarrhena asphodeloides.
    • Technique and Method
  • Construction and Application of the TUNEL-TSA Multiplex Fluorescent Staining Method Optimized Based on the TSA Technology
    HUANG Qiong, FANG San-Hua, YANG Dan, ZHANG Cheng-Cheng, YU Ya-Jun, ZHANG Li-Wen, LIU Lu, YIN Wei, ZHANG Hong-He
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1860-1869. https://doi.org/10.13865/j.cnki.cjbmb.2025.10.1118
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    Conventional terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) combined with multiplex fluorescence staining has its limitations, such as weak signals, suboptimal multicolor staining, and antibody species restrictions. Herein we introduced Tyramide Signal Amplification (TSA) technology to improve the TUNEL-based multiplex immunofluorescence staining method in a rat myocardial infarction model. We optimized the key parameters in the TUNEL staining system (proteinase K concentration: 8-15 μg/mL; incubation conditions: 37℃, 15 minutes) and the staining sequence. The research results demonstrated that when comparing the performance differences between conventional fluorescence staining and TSA fluorescence staining, the TSA technique significantly enhances fluorescence signal intensity while preserving more complete cellular morphological structures and overcoming antibody species limitations. In the multiplex staining procedure, the sequential protocol of "antigen retrieval → TSA fluorescence staining → proteinase K digestion → TUNEL staining" demonstrated significantly superior performance compared to the other two staining procedures, with its effectiveness validated in both mouse colon tumor and subcutaneous tumor models. In sum, the optimized TUNEL-TSA multiplex fluorescence labeling method exhibits significant signal enhancement, high structural integrity, excellent detection sensitivity and specificity, as well as strong antibody compatibility. Therefore, our research provides technical support for establishing a standardized in situ detection system for apoptosis-related immune factors, demonstrating broad prospects for clinical application.
    • Education and Teaching
  • Innovation and Practice of Experimental Teaching in “Introduction to Basic Medicine” Empowered by Digital Intelligence
    WANG Yan-Feng, SU Xiao-Min, ZHAO Guo-Xing
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1870-1882. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1465
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    Artificial intelligence (AI) is emerging as a pivotal technology that drives the high-quality development of medical education and teaching. The experimental teaching of “Introduction to Basic Medicine” for the Intelligent Medical Engineering faces various challenges, including outdated experimental content, insufficient depth in the teaching approach, challenges in integrating ideological and political education, and limited assessment criteria. The teaching team has implemented substantial measures, including the optimization of experimental teaching objectives, the integration of experimental teaching content in a three-dimensional framework, and the exploration of a human-intelligence collaborative smart teaching model. Additionally, they have developed an “intelligent body for ideological and political education in courses”, introduced AI assistance in teaching and management, and established a model of comprehensive composite evaluation for teaching and learning. These initiatives aim to enhance the innovation and practice of digital intelligence empowerment in the experimental teaching of “Introduction to Basic Medicine”. Practical experience indicates that this teaching model fosters students’ active learning and reflection, facilitates knowledge integration and construction, promotes transfer and application, encourages collaborative innovation, and enhances their sense of social responsibility. The effectiveness of this approach is noteworthy. With ongoing refinement, it is anticipated to significantly contribute to the development of multidisciplinary intelligent medical professionals.
  • Construction and Practice of a New Teaching Paradigm for Animal Cell Engineering Driven by Visual Design
    SUN Shao-Yi, PANG Yue, LU Jia-Li
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(12): 1883-1894. https://doi.org/10.13865/j.cnki.cjbmb.2025.11.1232
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    The course Animal Cell Engineering encompasses abstract and structurally intricate contents, addressing a range of molecular-level topics such as cellular proliferation, differentiation, and regulatory mechanisms, which are often challenging for students to fully comprehend. This study establishes a multi-dimensional teaching system by integrating static imagery for cellular structure analysis, dynamic visuals for demonstrating molecular mechanisms, virtual experiments for enhancing practical skills, and three-dimensional animal models for morphological recognition. Through the implementation of deeply interactive teaching strategies and the incorporation of aesthetic education principles, the course has effectively improved students’ understanding of complex mechanisms such as CRISPR-Cas9 and cellular metabolic pathways,and improved knowledge retention and classroom engagement. Teaching practice demonstrates that visual teaching methods substantially strengthen students' comprehension and memory of abstract knowledge, stimulate learning interest, and foster interdisciplinary literacy and innovative thinking. Furthermore, the introduction of design thinking and aesthetic education has expanded the humanistic connotation and aesthetic value of the course, providing a valuable reference for the reform of complex courses in higher education.
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