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    Mourn and Retrospect
  • JIA Hong-Ti
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 1-1.
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  • LI Zai-Ping
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 2-4.
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  • ZHANG Nai-Heng
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 5-8.
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  • Reviews
  • GUO Hao-Yan, CAI Rong, XING Rong
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 581-587. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.01
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    Nuclear factor erythroid 2 (NF-E2-related factor 2, Nrf2) is a master regulator of cellular responses against environmental or intracellular stresses, by regulating the expression of its target genes to mitigate oxidative stress under physiological conditions. Nrf2 is regulated by a variety of upstream factors including oxidative and electrophilic stresses, environmental nutrition status, metabolic intermediates and energy status in the cells, etc. Aberrant Nrf2 activation results in enhanced antioxidant capacities in cancer cells. Most importantly, Nrf2 promotes tumor cell proliferation and growth by reprogramming metabolism. The activity of Nrf2 is mainly regulated by Keap1, which acts as a sensor for oxidative and electrophilic stresses. In the present review, we mainly introduce the activation of Nrf2 in Keap1-dependent or -independent ways. We also emphasize aberrant activation of Nrf2 in the regulation of metabolic reprogramming in cancer, which in turn regulates the anabolism of tumor cells.
  • REN Xi-Ying, LIU Qin-Xian, WANG Hai-Ying
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 588-594. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.02
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    p53,an important tumor suppressor,is closely related to human cancers. More than 50% of human cancers contain p53 mutations. Thus, it is an important molecular target in cancer therapy. p53-dependent apoptosis is one of the important mechanisms of tumor suppression. However, recent studies have shown that p53 is not only involved in apoptosis but also associated with other types of cell deaths such as programmed necrosis, autophagy and iron-induced cell death (ferroptosis). Promoting tumor cell death is the ultimate goal of cancer therapies. Therefore, it is necessary to investigate the various functions of p53 in different modes of cell death, which will contribute to further studies on p53-targeted cancer therapy and p53-related tumor cell chemotherapy resistance.
  • LIU Jia-Jun, CHENG An-Chun, LIU Ma-Feng
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 595-603. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.03
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    Iron is an essential nutrient for most bacteria to survive, but excessive iron damages the bacteria through the Fenton reaction to produce reactive oxygen species (ROS). Thus, bacteria must strictly control the concentration of iron in vivo. Ferric uptake regulator (Fur) is the most important regulator of iron metabolism in bacteria. Fur regulates the genes involved in iron uptake, utilization and storage by repressing or activating gene transcription and balancing intracellular iron concentration. In addition, Fur is also involved in the regulation of various biological processes such as bacterial oxidative stress, acid resistance, virulence, energy metabolism and so on. In this review, we mainly discuss the biological processes regulated by Fur and its mechanism. It will provide a reference for further mechanistic studies on Fur and its role in the bacterial response to environmental changes.
  • WAN Lu, LIU Jie, SHI Chun-Wei
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 604-609. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.04
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    Exosomes are a type of extracellular vesicles that are released upon fusion of multivesicular bodies with the cellular plasma membrane. Exosomes are shown to deliver functional substances, including proteins, lipids and RNAs to recipient cells, mediating cell-to-cell communications and hence affecting the physiological and pathological functions of cells. In recent years, increased studies have found that exosomes play an important role in the pathogenesis of microbial infections. In chronic infection, pathogens have evolved strategies to spread infectious proteins and viral RNAs via exosomes to change the functions of uninfected cells. At the same time, proteins with high immunogenicity can deliver the pathogenic information to the immune system and hence activate anti-infectious immunity. This article reviews the progress of exosomes in microbial infections. Investigating these mechanisms may inspire future applications for the diagnosis and treatment of chronic infection.
  • LIAO Zi-Jie, YAN Yi-Hua, HU Xue-Feng
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 610-616.
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    Germinal centers (GCs) are transient convergences of lymphocytes and stromal cells that promote longlived humoral immunity within secondary lymphoid organs (SLOs). B cells undergo clonal expansion, somatic hypermutation (SHM), affinity selection and eventually differentiate into plasma cells (PCs) and memory B cells (B MEM) in GCs. However, the specific function of light zone and dark zone, and the mechanism by which B cells are selected remains unclear. Given the dynamic nature of GC, seminal application of intravital microscopy (IVM) has enabled the scientists to directly study GC features and make tremendous progress since the last decade. Recent studies show that B cell division and SHM are restricted to the DZ. Affinity selection is restricted to LZ and there is a net vector of B cell movement from the DZ to the LZ. Notably, the decision to return from the LZ to the DZ and undergo clonal expansion is controlled by T cells. In this paper, a series of dynamic reactions in GCs and their roles in vaccine design and disease treatment are reviewed.
  • LUAN Ming-Yue, JIN Yan, PIAO Cheng-Gang
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 617-621. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.06
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    SIRT1, a member of the Sirtuin family, is a class Ⅲ NAD+-dependent histone deacetylase that regulates gene expression by deacetylating lysine residues of various non-histone and histone proteins. Recent studies have found that SIRT1 not only deacetylates tumor suppressors, promotes tumorigenesis, but also deacetylates tumor-promoting factors and inhibits tumorigenesis. Furthermore, SIRT1 closely regulates the biological characteristics of tumors, affecting the tumor staging and prognosis of patients. In the tumors of the digestive system, SIRT1 has dual roles: a tumor suppressor, as well as a tumor promoter. In recent years, researchers have studied intensively the targets of SIRT1 in tumors and the related signal pathways, and have uncovered new mechanism of SIRT1 in tumors. SIRT1 has therefore become a hot research topic for tumor therapy. Here we review the dual roles of SIRT1 in tumorigenesis, in particular its distinct targets and the related signaling pathways in tumors of the digestive system, aiming provide more convincing evidence for clinical treatment.
  • Research Papers
  • SUN Liu-Liu, HUANG Fang-Ting, ZHANG Xu-Yan, ZHU Rui-Yu, JIN Jian
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 622-631. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.07
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    In addition to the traditional capdependent translation mechanism, eukaryotes also have internal ribosome entry site (IRES) that mediates translation mechanism. Estrogen receptor 2 (ESR2) is a member of estrogen receptor family and encodes protein that plays an important role in various types of tumor. Abnormal expression of ESR2 has been reported to induce tumorigenesis, but the regulation mechanism of ESR2 protein translation is still unclear. The expression of ESR2 protein was increased in MCF7/WT under drugstimulated condition, but its transcription level did not show significant difference. It is speculated that ESR2 mRNA 5′ untranslated region (5′ UTR) has an IRES activity. To verify whether the ESR2 mRNA 5′ UTR has IRES element, the ESR2 mRNA 5′ UTR was inserted into the double cistron reporter vector (pRF) to construct a pRL-ESR2-FL recombinant plasmid. The plasmid was transiently transfected into HEK293 cells. The results showed that ESR2 mRNA 5′ UTR had IRES activity. The ESR2 IRES activity was not related to its internal potential promoter (P<0.0001), internal alternative splicing site or ribosome read through by three exclusion experiments. Further truncation of the sequence showed that the key region of ESR2 IRES activity was 439-468 nt at three ends and the maximum activity of ESR2 IRES depended on the integrality of 5′ UTR sequence. It was also found that the activity of ESR2 IRES required not only a primary nucleic acid sequence, but also a stable secondary stem loop structure. This study is expected to provide new therapeutic targets for diseases related to the regulation of ESR2 protein.
  • WANG Yan,GUO Ming, FAN XiaoYue, BIAN PingFeng, YIN XinXin
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 632-641. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.08
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    The intermolecular interaction between naringin (NAR) and bovine serum albumin (BSA) was studied by fluorescence spectrum and microcalorimetry. The theoretical model of the interaction between NAR and BSA was established. Δ H, Δ S and Δ G were obtained by using the isothermal titration microcalorimetric technique and Gibbs-Helmholtz equation. The Fōrster equation was used to analyze the critical distance between NAR and BSA in the UV-fluorescence spectra. Based on spectroscopy- and microcalorimetry-assisted analysis, the theoretical model of the interaction between NAR and BSA was established. The critical distance between NAR and BSA was 2.06 nm, which indicated that the interaction between NAR and BSA was short-range intermolecular interaction. The results showed that the thermodynamic parameters Δ H <0, Δ S> 0 and Δ G <0 between NAR and BSA molecules have been successfully established by microcalorimetry. These microcalorimetry results showed that the interaction between NAR and BSA was spontaneous exothermic molecule interaction. According to the Ross theory analysis of NAR and BSA, intermolecular forces are mainly hydrophobic and electrostatic forces. Based on the analysis of UV-fluorescence spectra to obtain the binding distance, the intermolecular interactions between NAR and BSA were short-range. The theoretical model results showed that the intermolecular interaction of NAR and BSA occurred mainly in the domain IIA region of BSA. The NAR and BSA intermolecular forces are mainly electrostatic forces. Both van der Waals force and the presence of hydrogen bonds and the intermolecular interaction between BSA and NAR were a spontaneous process. The experimental results are basically consistent with the theoretical modeling results. These data can provide a useful reference for a comprehensive understanding of the intermolecular interactions between biological macromolecules and flavonoids and the study of microscopic pharmacological mechanisms.

  • HUANG Xu-Fang, ZHONG Jin-Man, ZHAO Wei-Wei, WEN Di-Di, REN Jing, HUAN Yi
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 642-648. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.09
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    Aptamers have great potential in the diagnosis and treatment of pancreatic cancer. Cell-SELEX(systematic evolution of ligands by exponential enrichment)is a common technique for screening cell-specific aptamers. This study aims to screen DNA aptamers that can specifically recognize pancreatic cancer cell line PANC-1 based on Cell-SELEX analysis. In this study, PANC-1 cells were used as positive cells, meanwhile HPDE6-C7 cells were used as negative cells. After 12 rounds of selection, the ssDNA pool was PCR-amplified and cloned, and monoclonal colony was selected for sequence analysis by Sangon Biotech. Results showed that DNA aptamers Apt-5 and Apt-12 were obtained. Flow cytometry was used to verify the affinity of the DNA aptamers with PANC-1 cells. Their Kd values were 8.27±2.10 nmol/L and 8.88±2.51 nmol/L, respectively. This study showed that the DNA aptamers screened by Cell-SELEX can specifically bind to PANC-1 cells, which may be used for finding potential molecular targets for the diagnosis and treatment of pancreatic cancer.
  • GUO Ji-Wei1) *, WU Yan,JIN Dan, DU Jing, GONG Kai-Kai,MIAO Shuang, YANG Li-Juan
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 649-658. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.10
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    Ubiquitin-conjugating enzyme E2C (UBE2C) is closely related to the proliferation of various tumor cells, but its relationship with the occurrence and development of lung cancer is not clear. The roles of UBE2C in cellular proliferation, cell senescence and migration of A549 lung cancer cells were elucidated by RT-PCR, Western blotting, immunofluorescence, SA-β-Gal cell senescence staining, cell scratch and Trans-well assays. Transient over-expression or targeted silencing of UBE2C by gene modification technique was used. The results showed that the expression of UBE2C in lung cancer cells was significantly higher than that in normal cells. The levels of UBE2C mRNA and protein were significantly increased by 3.5-fold or decreased by 0.5-fold in A549 cells after transient over-expression or silence of UBE2C, leading to significant promotion or inhibition of cell proliferation, thereby reducing or increasing the rate of apoptosis. In addition, over-expression of UBE2C significantly inhibited cell senescence, whereas silence of UBE2C promoted cell senescence. Moreover, UBE2C significantly affected the mRNA and protein expression of metastasis related genes E-cadherin and vimentin, and further modulated cell migration. This study provided information for the roles of UBE2C in the development and progression of lung cancer.

  • JI Xiao-Feng, ZHENG Yuan, WANG Zhi-Peng, SHENG Jun, WANG Hai-Ying
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 659-666. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.11
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    Marine protease (MP) is a new alkaline metalloprotease derived from marine bacteria and has a good application prospect in industry. The inhibitory effect of 4-formyl-phenyl-boronic acid (4-FPBA) on MP was studied by enzyme kinetic methods and combined with molecular dynamics simulation. The inhibitory mechanism was studied by molecular mechanics / poisson Boltzmann surface area(MM-PBSA)and quantum mechanics / molecular mechanics (QM/MM) methods in explicit water. The results showed that the inhibition process of 4-FPBA on MP is reversible competitive inhibition and the inhibition constant Ki is 0.57 mmol/L. Van Der Waals interaction plays an important role in the binding process of 4-FPBA and MP. Furthermore, four residues Arg59, Leu151, His190 and His196 were identified as the key residues mediating the binding between MP and 4-FPBA. These results provide a theoretical basis for the further screening and rational design of MP inhibitors, which would improve its stability in the liquid state and also provide better applications in liquid detergents.
  • GUO Wei, ZHANG Zhi-Jie, YIN Jiang, HE Zhi-Min
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 667-674. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.12
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    Serglycin (SRGN) plays a significant role in tumor invasion and metastasis. This study reports that SRGN specifically regulates invasion and metastasis of lung cancer. Firstly, we determined the expression levels of SRGN in the normal lung epithelial cell line BEAS2B and lung cancer cell lines 95C and 95D with different invasive and metastatic abilities. Then, using the shRNA method, we established a 95D/ShSRGN cell line, which stably knocks down SRGN expression in 95D cells. The knockdown efficiency was verified by RT-qPCR, Western blotting and ELISA. The results showed that interfering SRGN inhibits invasion and metastasis of 95D cells, upregulates the epithelial marker-epithelial cell cadherin (E-cadherin) and down-regulates the expression of fibronectin 1 (FN1) and zinc finger E-box binding homeobox 1 (ZEB1). Further analysis showed that SRGN negatively correlated with E-cadherin expression (P=-0.25) and positively correlated with FN1 (P=0.12) and ZEB1 (P=0.35). Clinically, the overall survival time of patients with SRGN overexpression was significantly lower (P=0.0077), and the overall survival of patients with high expression of SRGN and ZEB1 was significantly lower than that of patients with low expression of SRGN and ZEB1 (P=0.0005). In this study, we found that SRGN glycoproteins promote the occurrence of EMT, enhance the invasion and metastasis of non-small cell lung cancer cell lines, and provide a potential prognostic molecular marker for non-small cell lung cancer.
  • CHEN Wei-Quan, YANG Hong, TAN Guang-Mou, HUANG Hai-Yan, LIU Ke
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 675-680. https://doi.org/10.13865/j.cnki.cjbmb.2018.06.13
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    Small nucleolar RNA host gene 7 (SNHG7) is a long non-coding RNA (lncRNA). Recently, it was reported to be overexpressed in several kinds of cancers, thus it might function as an oncogene. However, its function in tongue cancer is still unknown. In this study, we carried out qRT-PCR assays and found that SNHG7 was downregulated in tongue cancer tissues and cells. Overexpression of SNHG7 inhibited the proliferation of tongue cancer cells, whereas downregulating SNHG7 got the opposite results. Bioinformatics analysis combined with dual luciferase reporter gene assays demonstrated that SNHG7-bound miR-9-5p reduced SNHG7 expression. Furthermore, overexpressing SNHG7 reduced miR-9-5p but upregulated autophagy / beclin 1 regulator 1 (Ambra1). Knocking down SNHG7 had the opposite results. According to the follow-up data of tongue tissue samples, we found that SNHG7 and Ambra1 positively correlated with the prognosis of tongue cancer patients, while miR-9-5p negatively correlated with the prognosis of tongue cancer patients. Thus, we suggest that SNHG7/miR-9-5p/Ambra1 can be used as potential biomarkers for tongue cancer prognosis.
  • HUANG Pei-Xiang, CHEN Li-Jun, MA Li, LI Li-Ping
    Chinese Journal of Biochemistry and Molecular Biol. 2018, 34(6): 681-688. https://doi.org/10. 13865/j.cnki.cjbmb.2018. 06. 14
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    Researches on the therapeutic effects of anticancer drugs mostly concentrated on tumor cells, but few studies were on normal cells. It is necessary to establish homologous recombination repair systems that can perform quantitative analysis. The models established can explore the secondary consequences of double-strand break (DSB) repair after chemotherapy on HEK293 cells. The effects of etoposide (VP-l6) on the homologous recombination (HR) pathway were quantitatively detected by constructing cell lines that contain homologous direct recombination (HDR) or single strand annealing (SSA) substrates with the I-SceⅠ restriction site. We successfully constructed normal human HEK293 cell models, which could be applied in the quantitative detection of DSB-induced SSA and HDR repairs. Cytotoxicity results confirmed that the cell viability of the VP-16-treated groups were significantly decreased at 16 μmol/L compared with the SSA/293 control groups (0.475±0.029 vs1.000±0.000, P<0.001), and decreased compared with the HDR/293 control groups (0.458±0.18 vs 81.000±0.000, P<0.05). In addition, this study confirmed that VP-16 inhibited SSA and HDR in HEK293 cells. The SSA repair efficiency was decreased in VP-16-treated groups at 2 μmol/L than the control SSA/293 cells (0.575%±0.177% vs 1.352%±0.195%, P<0.05), and the HDR repair efficiency was decreased in VP-16-treated groups at 1 μmol/L than the control HDR/293 groups (0.305% ± 0.078% vs 0.635% ± 0.049%,P<0.05). VP-16 induced DNA damages and inhibited HDR and SSA repairs, while their repair efficiencies were dosedependent. The results of this study may provide some guidance for the clinical application of anti-tumor drugs.