Jing-Jing Ren

Sichuan University, Hua-yang, Sichuan, China

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Publications (7)3.06 Total impact

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    ABSTRACT: Zinc finger proteins have been implicated as transcription factors in the differentiation and development of cells and tissues in higher organisms. The classical C2H2 zinc finger motif is one main type of motif of zinc finger proteins. Our previous studies have shown that Zfp637, which comprises six consecutively typical and one atypical C2H2 zinc finger motifs, is highly expressed in undifferentiated or poorly differentiated cell lines, but is moderately or slightly expressed in normal tissues. We have also demonstrated that Zfp637 can promote cell proliferation. However, its role in the regulation of cell differentiation remains unknown. We report here that endogenous Zfp637 as well as mTERT is expressed in proliferating C2C12 myoblasts and that their expression is downregulated during myogenic differentiation. Constitutive expression of Zfp637 in C2C12 myoblasts increased mTERT expression and telomerase activity, and promoted the progression of the cell cycle and cell proliferation. By contrast, endogenous repression of Zfp637 expression by RNA interference downregulated the mTERT gene and the activity of telomerase, and markedly reduced cell proliferation. Overexpression of Zfp637 also inhibited the expression of myogenic differentiation-specific genes such as MyoD and myogenin, and prevented C2C12 myoblast differentiation. Our results suggest that Zfp637 inhibits muscle differentiation through a defect in the cell cycle exit by potentially regulating mTERT expression in C2C12 myoblasts. This may provide a new research line for studying muscle differentiation.
    Journal of Cellular Biochemistry 03/2010; 110(2):352-62. · 3.06 Impact Factor
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    ABSTRACT: Na(+)-K(+)ATPase (Na(+)-K(+) pump) is an important cell energy conversion system which is probably associated with tumor metastasis. Expression of its B1 subunit gene-ATP1B1 is high in well differentiated and low in poorly differentiated tumor cells. This study was to investigate the synergic effect of Na(+)-K(+) ATPaseB1 and adriamycin (ADM) on inhibition of cell proliferation and reversal of drug resistance in MCF-7 and MCF-7/ADM cells. Growth of MCF-7 and MCF-7/ADM cells transfected with PEGFP-ATP1B1 and shATP1B1 were measured by MTT. Intracellular fluorescence intensity of ADM was analyzed by inverted fluorescence microscopy and flow cytometry. ATP enzyme activity was measured by ultramicro-ATP enzyme, and mRNA expression of multi-drug resistance gene MDR1 was detected by RT-PCR and real-time PCR. The expression of P-glycoprotein (P-gp) was analyzed by western blot. The sensitivity of MCF-7 and MCF-7/ADM cells transfected with pEGFP-ATP1B1 to ADM was higher in comparing to the negative control ADM-C3 (transfected with vector pEGFP-C3) and the control ADM-RPMI-1640 (cultured with RPMI-1640), and the differences between ADM-ATP1B1 and ADM-RPMI-1640 groups were statistically significant at different concentrations of adriamycin (P<0.05). After the B1 subunit was silenced, the sensitivity of cells to ADM in the ADM-shNC group was higher than that in the shATP and ADM-RPMI-1640 groups. The mean fluorescence intensity of ADM in the ADM-ATP1B1 group was higher than that in the ADM-C3 and ADM-RPMI-1640 groups (P<0.05). ATP enzyme activity was significantly higher in ADM-ATP1B1 group comparing to the ADM-RPMI-1640 group (P<0.05). mRNA expression of MDR1 gene and protein expression of P-gp were not significantly different among the ADM-ATP1B1 group and two control groups (P>0.05). Na(+)-K(+) ATPase B1 can synergize with ADM and reverse drug resistance to ADM in the MCF-7/ADM cell line. This may be related to ATP enzyme activity, but not to influencing the expression of MDR1 gene.
    Ai zheng = Aizheng = Chinese journal of cancer 08/2009; 28(8):861-7.
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    ABSTRACT: To construct the eukaryotic expression plasmid and establish stably transfected cell line, which contained the code gene of zinc finger protein637 (Zfp637), and to observe the effect of Zfp637 gene to the proliferation of tumor cells. The Zfp637 DNA was amplified from the template of normal spleen tissue cDNA and cloned into the eukaryotic expression vector pEGFP-C3. The recombinant plasmid, named as pEGFP-Zfp637, was determined by restriction enzyme and sequencing analyses. Next the pEGFP-Zfp637 recombinant plasmid was transferred into mouse breast carcinoma EMT6 cells with lipofectamine 2000, and the stably transfected cells were selected by G418 (named Zfp637-EMT6). The growth condition of cells was observed, and subcellular localization of Zfp637 gene was located by fluorescence microscope at the same time. The Zfp637 mRNA expression in the transfected cells was detected by RT-PCR, and the proliferation of such cells was measured by MTT. The analysis confirmed that the recombinant pEGFP-Zfp637 contained the Zfp637 full-length cDNA. The Zfp637 mRNA was over-expressed stably in Zfp637-EMT6. The growth of Zfp637-EMT6 was increased obviously when compared with the negative control group and blank group. The recombinant pEGFP-Zfp637 has been constructed successfully, and the expression of the Zfp637 gene can promote the proliferation of cells. This recombinant eukaryotic expression plasmid can be used in advanced studies in the biological effects of Zfp637 and anti-tumor gene therapy.
    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 07/2009; 40(4):575-8, 603.
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    ABSTRACT: The Na+/K+ ATPase B1 (ATP1B1) subunit gene is highly expressed in well-differentiated tumor cells, while it is hypoexpressed in poorly differentiated tumor cells. The expression of ATP1B1 is closely related to cell tight junction and polarity of epithelial cells. This study was to investigate the effect of specific interference of human Na+/K+ ATP1B1 using shRNA on cell proliferation and migration of gastric adenocarcinoma cell line SGC-7901. Four shRNA plasmids specifically targeting different fragments of ATP1B1, sh150, sh295, sh562, sh765, were constructed and transiently transfected into SGC-7901 cells. Stable positive clones, shATP1B1-7901 cells, were sorted out by G418. The expression of ATP1B1 mRNA was detected by semi-quantitative RT-PCR and real-time PCR. Cell proliferation was measured by MTT, cell cycle distribution was assessed by flow cytometry, and clone forming was analyzed by the colony formation assay. Cellular migration was observed using the Transwell experiment. At 24 h after transfection, the inhibition ratios of sh150, sh295, sh562, sh765 on ATP1B1 mRNA were (60.87+/-4.38)%, (44.93+/-2.24)%, (52.17+/-2.60)% and (52.17+/-2.60)% respectively in SGC-7901 cells, which were significantly higher than that of shNC control (3.00+/-0.15)%(p<0.05). Among the four ATP1B1 shRNAs, sh150 exerted the strongest effect (p<0.05) and was used in the following study. Assessed by RT-PCR and real-time PCR, the expression of ATP1B1 mRNA was inhibited by (85.72+/-5.22)% and (87.53+/-3.23)% in the shATP1B1-7901 group, in comparison with (3.3+/-0.22)% and (4.17+/-0.33)% in the shNC-7901 group (p<0.05). The proliferation ratio was higher in the shATP1B1-7901 group than in the shNC-7901 and SGC-7901 groups 3 days after transfection (p<0.05). Cells at S and G2/M phases in the shATP1B1-7901 group were significantly increased compared with those in the shNC-7901 and SGC-7901 groups (p<0.05). The clone formation rate of the shATP1B1-7901 group (68.50+/-2.65)% was higher than that of the shNC-7901 group (50.00+/-2.53)% and of the SGC-7901 group (52.50+/-2.11)% (p<0.05). Moreover, the migration ratio of the shATP1B1-7901 group(2.80+/-0.02)% was significantly enhanced comparing to the shNC-7901 (1.15+/-0.05)% and the shNC-7901 groups (1.25+/-0.02)% (p<0.05). Silencing of ATP1B1 gene can enhance the proliferation and migration capability of SGC-7901 cells.
    Ai zheng = Aizheng = Chinese journal of cancer 04/2009; 28(3):225-31.
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    ABSTRACT: To establish the eukaryotic expression plasmid containing the code gene of Na+, K+-ATPase beta1-subunit (ATP1B1) and the basis of ATP1B1 applied to antitumor gene therapy. The ATP1B1 cDNA was amplified from leukocyte gene library and then cloned into the eukaryotic expression vector pEGFP-C3. The recombinant plasmid, named as pEGFP-ATP1B1, was determined with restriction enzyme and sequencing analyses. Next pEGFP-ATP1B1 was transferred into gastric adenocarcinoma SGC-7901 cells by lipofectamine, then ATP1B1 mRNA expression in transfected cells was detected by real-time PCR, and also ATPase was detected after cell transfection, as well as the proliferation of such cells was measured by MTT. The analysis confirmed that the recombinant pEGFP-ATP1B1 contained the ATP1B1 cDNA. After cell transfection, the expression of ATP1B1 mRNA(129.2%) and the activity of ATPase [(2.95+/-0.210)%] were higher, and the growth of the SGC-7901 cells transfected with ATP1B1 was inhibited obviously when compared with the control group. The recombinant pEGFP-ATP1B1 is constructed successfully, and this recombinant eukaryotic expression vector could be used in additional studies on the biological effect of ATP1B1 and its use in anti-tumor gene therapy.
    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 03/2008; 39(2):169-72, 176.
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    ABSTRACT: To detect the relation between the member LIGHT of TNF superfamily and the suppressor of cytokine signaling 3 (SOCS3), and to investigate the effect of SOCS3 on dendritic cell (DC) maturation induced by LIGHT. Bone marrow-derived DC (BMDC) was generated from mouse bone marrow monocyte by culturing with rmGM-CSF, rmIL-4 in vitro. SOCS3 mRNA in BMDC was analyzed by RT-PCR, and the protein of SOCS3 was measured by Western blot. After blocking the SOCS3 expression with the specific anti-sense oligonucleotide, we applied the flow cytometry to measure the expression of CD86 and CD40 on DC for making clear whether the silence of SOCS3 would regulate the LIGHT-stimulated DC maturation. With the effect of LIGHT, the level of SOCS3 mRNA and protein in BMDC sharply increased. The specific antisense oligonucleotide could effectively block SOCS3 mRNA expressing in BMDC with the ratio of 49% and block SOCS3 protein expression with the ratio of 45%. Compared with SOCS3-unblocked DC, the SOCS3-blocked BMDC with stimulation of LIGHT showed higher CD40 and CD86 (P < 0.05). LIGHT enhances the expression of SOCS3 during stimulating BMDC maturation. As more sensitive to LIGHT, the SOCS3-blocked BMDC is driven to more mature. SOCS3 presents a negative regulation mechanism in BMDC maturation induced
    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 07/2007; 38(4):644-8.
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    ABSTRACT: To investigate the growth inhibition and multidrug resistance (MDR) reversing effect of tanshinone I A on human breast cancer cells with estrogen receptor (ER) negative, and to elucidate its mechanism of activity. Human ER negative breast cancer cells (MDA-MB-231) were tested in vitro for cytotoxicity and colony formation inhibition. Brdu incorporation and cell cycle distribution were also checked through flow cytometry (FCM). With RT-PCR, the expressions of ADP-ribosyltransferase CNAD+; poly (ADP-ribose) polymerase)-like 1 (ADPRTL1), cytochrome P450 subfamily I (CYP1A1) and breast cancer resistance protein (BCRP/ABCG2) mRNA were detected for testing the response to tanshinone 1 A treatment. After tanshinone I A treatment, the proliferation, colony formation and Brdu labeling indices of cancer cells decreased (P<0. 05). By FCM analysis, the increase of subG, and G0/G1 phase cell populations and decrease of S and G2/M phase cells were observed (P<O. 01), both ADPRTL1 and CYP1A1 mRNA expression increased (P< 0. 05), while BCRP/ABCG2 mRNA expression was decreasing (P<0. 05). The findings in these studies suggest that tanshinone I A exhibits the potent cytotoxicity and MDR reversing potential to human ER negative breast cancer cells. The mechanism for such effects may be associated with the inhibition of DNA synthesis, induction of apoptosis, cell cycle arrest and up-regulation of ADPRTL1, CYP1A1, and down-regulation of BCRP/ABCG2 expression in cancer cells.
    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 06/2007; 38(3):391-5.