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1.
AIM: To investigate the molecular mechanism of hepatitis C virus (HCV) chronic infection by studying the effect of its core protein on cell growth and the expression of cell cycle regulators such as cyclin D1 and pRb/p130 in HepG2 cells. METHODS: A eukaryotic expression vector that carried a gene encoding HCV-core-1b was constructed. The cDNA of HCV core protein was subcloned into pBabe-Flag-puro vector to generate pBabe-Flag-HCV-core-1b. The plasmid was transfected into Pheonix 293T packaging cells to produce retroviruses. The virus-containing supernatant collected from the cell culture was used to infect HepG2 cells and subsequently the cell line that stably expressed the core protein of HCV was obtained.The cell cycle was analyzed by flow cytometry. The expression of cyclin D1 and pRb/p130 was examined by Western blotting. RESULTS: The pBabe-Flag-HCV-core-1b vector was confirmed by DNA sequencing. The expression of HCV gene type 1b core protein was verified by Western blotting. The overexpression of HCV gene type 1b core protein impaired the cell cycle progression in G0/G1 phase and significantly reduced the levels of cyclin D1 and pRb/p130 in the cells. CONCLUSION: A eukaryotic expression plasmid that contains the cDNA of HCV core protein is successfully constructed, and a HepG2 cell line which stably expressed the core protein of HCV is also established. HCV gene type 1b core protein inhibits the cell cycle possibly through down-regulation of cyclin D1 and pRb/p130 proteins in the cells.  相似文献   

2.
AIM: To investigate the oncogenic effect of microRNA-106a (miR-106a) on normal gastric mucous epithelial cells and gastric cancer cells.METHODS: The miR-106a mimic was transfected into normal gastric mucous epithelial cell line GES-1 using liposome. The change of cell growth was measured by MTT assay. The miR-106a inhibitor was transfected into gastric cancer cell lines MGC-803 and SGC-7901 using liposome, and the changes of cell cycle distribution and cell cycle-related protein expression were measured by flow cytometry and Western blotting,respectively. The growth of gastric cancer was also observed using nude mouse xenograft model. RESULTS: The miR-106a mimic increased the growth of GES-1 cells in a dose-dependent manner. By decreasing the expression of cyclin-dependent kinase (CDK) 1 and CDK2, the miR-106a inhibitor arrested MGC-803 cells at G0/G1 and G2/M phases. The miR-106a inhibitor also arrested SGC-7901 cells at G2/M phase by decreasing the expression of CDK1. The results of animal experiments showed that the miR-106a inhibitor significantly suppressed the tumor growth in a dose-dependent manner.CONCLUSION: miR-106a may play an important role in the development of gastric cancer.  相似文献   

3.
AIM: To explore the effect of SET and MYND domain-containing protein 3 (SMYD3) over-expression on the expression of DNA methyltransferase 3B (DNMT3B) and the proliferation ability in human cholangiocarcinoma cell line FRH0201. METHODS: Transient transfection of SMYD3 eukaryotic expression plasmid pEGFP-C3-SMYD3 into human cholangiocarcinoma cell line FRH0201 was performed. The expression of DNMT3B at mRNA and protein levels was detected by RT-PCR and Western blotting,respectively. Cell proliferation was examined by CCK-8 method and cell cycle situation was checked by flow cytometry. RESULTS: After transfected with SMYD3 eukaryotic expression plasmid pEGFP-C3-SMYD3, the over-expression of SMYD3 in FRH0201 cells was observed. Compared with the untransfected cells, the expression of DNMT3B was significantly increased (P<0.01), the proliferation rate was obviously accelerated (P<0.05) and the number of the cells in G2/M phase was significantly increased (P<0.05) in FRH0201 cells transiently transfected with pEGFP-C3-SMYD3 plasmid. CONCLUSION: The transient transfection of pEGFP-C3-SMYD3 plasmid induces over-expression of DNMT3B and promotes the proliferation of human cholangiocarcinoma cell line FRH0201.  相似文献   

4.
AIM: To investigate the method of inducing G1 phase synchronization in human endometrial cancer JEC Cells by lovastatin and the cell cycle progress of JEC cells after desynchronization. METHODS: The doubling time of JEC cells was detected by Cell Counting Kit-8 (CCK-8) assay. To determine the best lovastatin concentrations for G1 synchronization, JEC cells were treated with lovastatin at concentrations of 10, 20, 30 and 40 μmol/L for 1× doubling time, and the cell cycle was detected using flow cytometry (FCM). To determine the best period of lovastatin treatment to achieve G1 synchronization, JEC cells were treated with lovastatin at the best concentration for 0.5× to 2× doubling time, and the cell cycle was detected every 4 h using FCM. Furthermore, the cell cycle progress of JEC cells after desynchronization was also observed. RESULTS: The doubling time of JEC cells was almost 24 h. Treatment with lovastatin at the concentration of 20 μmol/L for 24 h achieved maximum G1 arrest in JEC cells. Minimum G1 phase and maximum S phase were observed after desynchronization for 16 h. CONCLUSION: Maximum G1 synchronization of JEC cells is induced by lovastatin at the concentration of 20 μmol/L for 24 h. The JEC cells show minimum G1 phase and maximum S phase after desynchronization for 16 h.  相似文献   

5.
AIM: To explore a new gene therapeutic strategy for vein graft restenosis by investigating the effects of adenovirus-mediated human growth arrest-specific homeobox (Ad5-hGax) gene delivery on the proliferation, migration and cell cycle distribution of serum-induced rabbit vascular smooth muscle cells (VSMCs). METHODS: The recombinant adenovirus vector containing hGax gene was constructed and transfected into rabbit VSMCs. The expression of hGax in VSMCs was detected by RT-PCR and immunofluorescent staining. Methyl thiazolyl tetrazolium (MTT) assay was used to assess the effect of hGax over-expression on serum-induced proliferation of VSMCs. Wound healing method was applied to examine the distance of serum-induce VSMCs migration. Flow cytometry was employed to analyze the cell cycle distribution. RESULTS: The recombinant adenovirus vector Ad5-hGax was successfully constructed. The results of RT-PCR and immunofluorescent staining revealed that the hGax -transfected cells contained a 174 bp specific fragment of hGax gene and target protein 48 h after transfection. The proliferation of serum-induced VSMCs was significantly inhibited by overexpression of hGax gene as compared with control group. The migration of serum-induced VSMCs was inhibited after hGax gene delivery. Flow cytometry showed that 72 h after serum induction, the cells in G0/G1 phase in Ad5-hGax group were significantly increased, whereas the cells in G2/M+S phase were significantly decreased. CONCLUSION: Overexpression of hGax gene inhibits the proliferation and migration of serum-induced rabbit VSMCs, and arrests the cells in G0/G1 phase. It is likely that hGax gene is a potential target for the gene therapy of vein graft restenosis.  相似文献   

6.
AIM: To investigate the effect of siRNA-induced astrocyte elevated gene-1 ( AEG-1 ) down-regulation on the proliferation, apoptosis and cell cycle of neuroblastoma cells. METHODS: An siRNA targeting to AEG-1 mRNA (AEG-1 siRNA) was constructed and transfected into neuroblastoma cells with Lipofectamine 2000. A non-specific siRNA (control siRNA) and non-treatment were used as negative control and blank control,respectively . The cell proliferation was detected by MTT method and colony formation assay. The apoptosis and cell cycle were analyzed by flow cytometry. RESULTS: Compared with control groups, the expression of AEG-1 mRNA was evidently declined in the cells transfected with AEG-1 siRNAs (P<0.05). AEG-1 siRNA significantly decreased the cell proliferation. After treated with AEG-1 siRNA for 48 h, the percentage of apoptotic cells was significant increased and the cell cycle was arrested in G0/G1 phase compared with the control cells (P<0.05). CONCLUSION: The mRNA expression of AEG-1 is down-regulated by AEG-1 siRNA in neuroblastoma cells. Knockdown of AEG-1 expression in human neuroblastoma cells significantly inhibits cell proliferation and apoptosis, and induces cell arrest in G0/G1 phase of the cell cycle.  相似文献   

7.
AIM: To investigate the effects of shRNA-mediated collagen type I alpha 1 (COL1A1) gene silencing on the proliferation and apoptosis of human breast cancer cell line MDA-MB-231. METHODS: The specific recombinant vector pSilencer2.1-U6-COL1A1 was transiently transfected into human breast cancer cell line MDA-MB-231 with lipofectamine. RT-PCR and Western blotting were performed to detect the expression levels of COL1A1. MTT assay was employed to evaluate the effect of COL1A1 gene silencing on the cell proliferation. Flow cytometry was used to determine the apoptosis and cell cycle of transfected cells. The morphological characteristics of apoptosis were observed by Hoechst 33258 staining. RESULTS: Compared with mock group and scrambled group, the mRNA and protein levels of COL1A1 were reduced by pshRNA-COL1A1 transfection (P<0.05). The proliferation of MDA-MB-231 cells treated in shRNA-COL1A1 was significantly inhibited in a time-dependent way. The percentages of G0/G1 phase cells and early apoptotic rate were significantly higher in pshRNA-COL1A1 group than those in mock and scrambled group (P<0.05). The changes of apoptotic morphology such as cell shrinkage and nuclear condensation were also observed by staining with Hoechst 33258 under fluorescence microscope. CONCLUSION: Transfection of eukaryotic expression vector pshRNA-COL1A1 effectively inhibits the proliferation, induces apoptosis and arrests MDA-MB-231 cells in G0/G1 phase.  相似文献   

8.
AIM: To investigate the effects of human xeroderma pigmentosum group D (XPD) gene on the proliferation of human vascular smooth muscle cells (VSMCs) induced by interleukin-6 (IL-6). METHODS: Recombinant plasmid pEGFP-N2/XPD and vacant plasmid pEGFP-N2 were transfected into VSMCs by liposome, and then these cells were incubated with IL-6 at 1×105 U/L for 48 h. The cells were divided into 6 groups: blank control group; pEGFP-N2 group; pEGFP-N2/XPD group; IL-6 group; IL-6 + pEGFP-N2 group; IL-6 + pEGFP-N2/XPD group. The expression of green fluorescent protein was observed under fluorescence microscope. The cell growth was detected by MTT method. The cell cycle and apoptosis rate were examined by flow cytometre. The expression levels of XPD, Bcl-2, Bax and wild type P53 (wt-P53) were detected by RT-PCR and Western blotting.RESULTS: Green fluorescence was observed in the cells transfected with pEGFP-N2/XPD or pEGFP-N2, indicating successful transfection MTT results showed that the transfection of pEGFP-N2/XPD inhibited the cell growth, and reduced the positive effects of IL-6 on VSMCs growth. Flow cytometry results showed that the transfection of pEGFP-N2/XPD increased the apoptosis rate of VSMCs and the cell numbers in G0/G1 phase, decreased the cell numbers in S phase, and reduced the effects that IL-6 decreased the apoptosis rate of VSMCs and the cell numbers in G0/G1 phase, and increased the cell numbers in S phase. The results of RT-PCR and Western blotting showed that the transfection of pEGFP-N2/XPD increased the expression of XPD, Bax and wt-P53, decreased the expression of Bcl-2, and reduced the effects that IL-6 decreased the expression of Bax and wt-P53, and increased the expression of Bcl-2. CONCLUSION: XPD gene inhibits VSMCs proliferation, promotes VSMCs apoptosis, and reduces the effects that IL-6 promotes VSMCs proliferation and inhibits VSMCs apoptosis. Therefore, XPD gene is likely to be potential molecular target for treatment of atherosclerosis.  相似文献   

9.
AIM: To investigate the effect of small interfering RNA (siRNA)-mediated ABCE1 knockdown on the survival, cell cycle and invasion of human bladder cancer cell line T24. METHODS: The siRNA against ABCE1 was constructed and transfected into the T24 cells with LipofectamineTM 2000. The expression of ABCE1 was detected by RT-PCR and Western blot. Flow cytometry was used to detect the cell cycle. The effects of ABCE1 gene silencing on proliferation, migration and invasion of T24 cells were evaluated by CCK-8 assay, wound-healing assay and Transwell invasion assay, respectively. RESULTS: Compared with control group and blank group, the mRNA and protein levels of ABCE1 were significantly decreased in experimental group after transfected with ABCE1 siRNA. The cell cycle was arrested at G0/G1 phase and the cell number in S phase was decreased in the T24 cells. Compared with control group and blank group, the proliferation of T24 cells in experimental group was inhibited significantly, and the migration and invasion abilities of T24 cells in experimental group decreased significantly. CONCLUSION: Knockdown of ABCE1 gene may decrease migration, invasion and proliferation abilities in T24 cells.  相似文献   

10.
AIM: To study the effect of hexamethylene bisacetamide(HMBA) on the proliferation and expression of KLF6 and related proteins in human tongue carcinoma Tca8113 cells. METHODS: After cultured with HMBA, the growth of the Tca8113 cells was assayed by MTT method, and the morphology of the cells was observed under microscope. The cell cycle was determined by flow cytometry. The mRNA expression of KLF6 was detected by RT-PCR. The protein levels of KLF6, p53, cyclin D1 and c-Jun were measured by the method of immunohistochemistry. RESULTS: The number of adherent cells obviously decreased along with the concentration of HMBA, and the growth inhibition of Tca8113 cells was in a concentration/time-effect relationship after treated with HMBA. Some reversal features of the Tca8113 cells developed to normal cells in morphology after induced by HMBA. The proportion of the cells in G1 phase was (52.00?0.02)% before treating with HMBA. The proportion of the cells in S phase was (34.00?0.08)%, and (14.00?0.10)% of G2 phase cells. After treated with HMBA, the cell number in G1 phase significantly increased with the exposure time going on, while the cell number in S phase significantly reduced, so did the cell number in G2 phase. The cell cycle was significantly arrested in G1 phase (P<0.05). The apoptosis peak also appeared. The mRNA expression of KLF6 significantly increased after induced by HMBA (P<0.05), so did the protein levels of KLF6 and p53 (P<0.05), while the expression of cyclin D1 and c-Jun was significantly decreased (P<0.05). CONCLUSION: HMBA inhibits the proliferation of Tca8113 cells by arresting the cell cycle in G0/G1 phase and resuming Tca8113 cells to normal and apoptosis at last.  相似文献   

11.
AIM: To study the effect of hypoxia-inducible factor 1α(HIF-1α) silencing on the expression of p27 and Ki67 in rat hepatoma cell line CBRH-7919 under hypoxia. METHODS: Hypoxic condition was induced by CoCl2 and the expression of HIF-1α was silenced by small interference RNA. HIF-1α-specific RNAi lentiviral vector was constructed. Real-time RT-PCR and Western blotting were used to detect the expression of HIF-1α at mRNA and protein levels in CBRH-7919 cells under hypoxia. The expression of p27 and Ki67 was observed by Western blotting after HIF-1α silencing was performed. The cell cycle of hepatoma cells was detected by flow cytometry. RESULTS: Under hypoxic condition, the expression of HIF-1α at mRNA and protein levels in CBRH-7919 cells increased significantly (P<0.05). HIF-1α silencing significantly reduced the expression of Ki67 but increased the expression of p27 (P<0.05) in CBRH-7919 cells. In transfected cells, the number of cells in G0/G1 phase was much higher and that in S phase was much lower than those in the control cells. CONCLUSION: Hypoxia induces the expression of HIF-1α. HIF-1α silencing can regulate the proliferation of hepatoma cells through reducing the expression of Ki67 and increasing the expression of p27.  相似文献   

12.
AIM:To investigate the relationship between Sonic Hedgehog (Shh) signaling pathway and cell cycle and radioresistance of esophageal cancer by up-regulating Gli1, a key factor in Shh signaling pathway. METHODS:The human esophageal cancer cell line Eca109 was transfected with plasmid to induce Gli1 over-expression, which served as Eca109-ox-Gli1 group. In addition, Eca109 cells transfected with empty plasmid served as negative control group and the untreated Eca109 cells were used as normal control group. The expression of Gli1 was confirmed by real-time PCR and Western blot. The radiosensitivity of the cells in the 3 groups was determined by colony formation assay. The effect of irradiation on the cell cycle was analyzed by flow cytometry. RESULTS:The expression of Gli1 in Eca109-ox-Gli1 group was higher than that in the other 2 groups (P<0.05). The survival fraction at dose of 2 Gy in Eca109-ox-Gli1 group was higher than that in normal control group, indicating that the radioresistance of the Eca109 cells transfected with Gli1 plasmid was increased. The cells in Eca109-ox-Gli1 group showed higher S phase proportion than that in normal control group and negative control group (P<0.01). After irradiation at dose of 6 Gy, all cells in the 3 groups found that the cell cycle was arrested at G2/M phase, while the cells in normal control group showed higher G2/M phase proportion than that in Eca109-ox-Gli1 group (P<0.01). CONCLUSION:The up-regulation of Gli1 may enhance the radioresistance of esophageal cancer by regulating the cell cycle.  相似文献   

13.
AIM: To investigate the effect of small interfering RNA(siRNA) on limb-bud and heart(LBH) gene expression in 16HBE cells, and further to observe the change of 16HBE cell cycle after knocking down of LBH gene. METHODS: Synthetical siRNA targeting LBH gene was transfected into 16HBE cells by the method of lipofectamine 2000. The mRNA expression of LBH was examined by real time RT-PCR. The cell cycle was assayed by flow cytometry. The expression of cyclin E1 and E2 was also detected by real time RT-PCR and Western blotting.RESULTS: The expression of LBH gene decreased by 86% in 16HBE cells transfected with 50 nmol/L of siRNA for 48 h. After transfected with siRNA for 48 h, 16HBE cells in G1 phase decreased by 9.28% and the cells in S phase increased by 14.08%. The expression level of cyclin E2 in 16HBE cells transfected with siRNA was twice higher than that of the negative control cells.CONCLUSION: Sequence-specific siRNA targeting LBH is capable of suppressing LBH gene expression in 16HBE cells. Down-regulation of LBH expression in 16HBE cells may promote the progress of cell cycle, and up-regulation of cyclin E2 expression plays a role in the process of G1/S phase.  相似文献   

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15.
AIM:To investigated the effect of 7-hydroxyisoflavone (7-HIF) on the proliferation, apoptosis and stem-like cell feature of colorectal cancer cells. METHODS:The effect of 7-HIF on the proliferation of HCT116 cells was detected by WST-1 assay and colony formation assay. The effects of 7-HIF on the cell cycle distribution and apoptosis in the HCT116 cells were analyzed by flow cytometry. The expression of cell-cycle related proteins and the stemness related proteins was determined by Western blot. RESULTS:After treated with 7-HIF (200 μmol/L), the viability of HCT116 cells was inhibited, and the size and number of the colony were decreased as compared with control group (P<0.05). The G0/G1 phase of the cell cycle was increased. The proportion of S phase was decreased and the cells were mainly arrested in G0/G1 phase. The apoptotic rate of HCT116 cells was 21.4%, which was significantly higher than that in the control group (1.1%). The results of Western blot revealed that the expression of inhibitor of differentiation 1(Id1) was significantly decreased (P<0.05). The expression of cell cycle markers cyclin D1 and cyclin E, the proliferative markers survivin and PCNA, and stem cell markers CD133, ALCAM and EpCAM were all down-regulated by 7-HIF treatment (P<0.05). CONCLUSION:7-HIF inhibits the proliferation and induces the apoptosis of colorectal cancer cells, and inhibits the stem-like cell feature, which may be related to Id1 inhibition.  相似文献   

16.
AIM: To analyze the difference of endonuclease domain containing 1 (ENDOD1) expression between benign prostatic hyperplasia (BPH) tissues and prostate cancer (PCa) tissues and to investigate the effect of ENDOD1 on the biological function of human prostate cancer cells. METHODS: The BPH samples (n=20) and PCa samples (n=21) were processed and analyzed according to the instruction of immunohistochemical (IHC) staining. The mRNA and protein levels of ENDOD1 in the normal prostate epithelial cells and prostate cancer cells were evaluated by RT-qPCR and Western blot, respectively. The recombinant plasmids pCMV-N-Flag-ENDOD1 was constructed and was transfected into the human prostate cancer cells. The proliferation, apoptosis, migration and invasion abilities of the prostate cancer cells were evaluated by MTT assay, flow cytometry, Transwell migration and Matrigel invasion assays, respectively. RESULTS: The analysis of variance of the immunoreactivity score showed that PCa tissues with high Gleason score displayed significantly lower ENDOD1expression than that with low Gleason score and BPH (P<0.05). The expression of ENDOD1 at mRNA and protein levels in PC3 cells and DU145 cells was significantly lower than that in the LNCap cells (P<0.05). The proliferation of DU145 transfected with ENDOD1 was inhibited. The flow cytometry indicated that ENDOD1 over-expression in the DU145 cells resulted in a notable increase in G0/G1 phase arrest (P<0.05), but the apoptotic rates showed no statistical difference. The results of Transwell assay showed that migration and invasion abilities of the cells were also inhibited after transfection with over-expressing ENDOD1 plasmid (P<0.05). CONCLUSION: The expression of ENDOD1 significantly decreased in prostate cancer with high Gleaon score. Meanwhile, the ENDOD1 is specifically down-regulated in androgen independent prostate cancer (AIPC) cell lines. Over-expression of ENDOD1 remarkably inhibits the proliferation, migration and invasion abilities of AIPC.  相似文献   

17.
AIM: To study the expression of eukaryotic elongation factor 1A2 (eEF1A2) in the hepatocellular carcinoma (HCC) tissues and the effects of eEF1A2 over-expression on the biological behaviors of the HCC cells. ME-THODS: The expression of eEF1A2 at mRNA and protein levels in the HCC tissues and matched liver tissues from 62 HCC patients, and 20 normal liver tissues were detected by the methods of real-time PCR and immunohistochemical staining, respectively. The mRNA and protein expression of eEF1A2 in the HCC cells was also determined by real-time PCR and Western blot, respectively. The lentivirus containing eEF1A2 gene was constructed, and was used to infect the HCC cells with low eEF1A2 expression. The expression of eEF1A2 at mRNA and protein levels in the infected cells was detected by real-time PCR and Western blot, respectively. The cell activity, cell cycle and mRNA expression of albumin were measured by MTT assay, DNA ploid analysis and real-time PCR, respectively.RESULTS: The mRNA expression levels and protein expression positive rates of eEF1A2 in the 62 cases of HCC tissues, were significantly higher than those of 62 matched liver tissues and 20 normal liver tissues (P<0.01). eEF1A2 mRNA and protein were highly expressed in SMMC-7721 cells and BEL-7402 cells, and expressed in SK-HEP-1 cells at low level. The expression of eEF1A2 at mRNA and protein levels in the SK-HEP-1 cells was significantly enhanced by infection of GV287-eEF1A2 expression lentivirus.Compared with negative control group (transfected with negative control lentivirus), the cell activity in eEF1A2 over-expression group (transfected with GV287-eEF1A2 expression lentivirus) was significantly enhanced, the mRNA expression of albumin was remarkably reduced, and the cells in G0/G1 phase were significantly decreased with increased percentage of the cells in S and G2/M phases.CONCLUSION: eEF1A2 is selectively over-expressed in human HCC cancer tissues. eEF1A2 might be a putative oncoprotein in HCC. eEF1A2 over-expression has noticeable effects on the HCC cell proliferation enhancement, differentiation inhibition, and cell cycle acceleration through the G0/G1 phase to S phase and G2/M phases.  相似文献   

18.
AIM: To investigate the mechanism that insulin-like growth factor binding protein 7 (IGFBP7) inhibits proliferation of human breast cancer cell line MCF-7. METHODS: Plasmid pCMV6-IGFBP7 or empty plasmid was transfected into MCF-7 cells. The expression of IGFBP7 in MCF-7 cells after transfection was detected by Western blotting. The effects of IGFBP7 on the colony-forming efficiency and the cell cycle were studied by soft agar colony formation assay and flow cytometry,respectively. The effects of IGFBP7 on the expression of ERK1/2, p-ERK1/2, cyclin D1, CDK4, cyclin E, CDK2, p21CIP1/WAF1, p27KIP1, p53, Rb and p-Rb in MCF-7 cells were detected by Western blotting. RESULTS: Only the transfectant of pCMV6-IGFBP7 expressed IGFBP7. IGFBP7 remarkably reduced colony-forming efficiency (P<0.01) and G0/G1 arrest (P<0.01), inhibited phosphorylation of ERK1/2 (P<0.01), down-regulated cyclin D1 and cyclin E (P<0.01), up-regulated p27KIP1, p21CIP1/WAF1 and p53 (P<0.01), and inhibited phosphorylation of Rb (P<0.01) in MCF-7 cells. PD98059, an inhibitor of MEK1 and MEK2, imitated part of the tumor-suppressing activity of IGFBP7. CONCLUSION: IGFBP7 inhibits the proliferation of human breast cancer cell line MCF-7 by down-regulating cyclin D1 and cyclin E, up-regulating p27KIP1, p21CIP1/WAF1 and p53 and inhibiting phosphorylation of Rb. ERK1/2 signaling pathway might be involved in the regulation of cyclin D1 and p27KIP1 by IGFBP7.  相似文献   

19.
AIM: To investigate the effect and mechanism of sodium selenite (Na2SeO3) on the proliferation of endometrial cancer cells. METHODS: Endometrial cancer Ishikawa cells and HEC-1A cells were treated with Na2SeO3. The effect of Na2SeO3 on cell proliferation was determined by MTT assay. The effects of Na2SeO3 on cell cycle distribution and apoptosis were tested by flow cytometric analysis. The expression of cyclin A was detected by Western blotting. RESULTS: Na2SeO3 inhibited the proliferation of Ishikawa cells and HEC-1A cells. For Ishikawa cells, IC50 was 3.26 μmol/L, and for HEC-1A cells, IC50 was 4.77 μmol/L. After treated with Na2SeO3, the cells in G0/G1 phase were reduced and the cells in S phase and G2/M phase were increased. Na2SeO3 also increased the percentage of apoptosis cells. The result of Western blotting showed that the expression of cyclin A was increased. CONCLUSION: Na2SeO3 inhibits the proliferation of endometrial cancer Ishikawa cells and HEC-1A cells via up-regulating the expression of cyclin A, arresting cell cycle and inducing apoptosis.  相似文献   

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