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1.
AIM:To observe the effect of protein kinase C-α(PKCα)antisense oligonucleotide on cell growth, cell cycle and the expression of cyclin E in human poor-differentiated nasopharyngeal carcinoma(NPC) cell line CNE-2Z. METHODS:Antisense PKCα was transfected by cationic liposome(LP) in CNE-2Z cells to analyze the cell growth and cell cycle by MTT colorimetric assay and flow cytometry, respectively. Moreover, the expression of cyclin E was determined by immunocellularchemistry and scanning the result of dot-blotting. RESULTS:①With the concentration of antisense PKCα increasing, the relative cell growth index was decreased gradually(P<0.01). ②After treated with antisense PKCα, the percentage of cells in G1 phase enhanced(P<0.05). ③Compared with the control group, the expressing intensity of cyclin E reduced in antisense PKCα group, and the expression of cyclin E decreased to 66.5%±18.4%(P<0.05) of the control by scanning quantitative analysis. CONCLUSION:These results indicated that antisense PKCα may inhibit cell growth in CNE-2Z via suppressing the expression of cyclin E and hindering cell process in G1 phase.  相似文献   

2.
AIM: To study the roles of ClC-3 chloride channel in the inhibition of nasopharyngeal carcinoma cell cycle by metformin. METHODS: The CNE-2Z cells were treated with metformin at different concentrations. The viability of CNE-2Z cells was measured by CCK-8 assay. The cell cycle distribution was detected by flow cytometry. The protein expression of ClC-3 was determined by Western blot. The Cl- currents was record by the patch-clamp technique. In addition, the cell cycle distribution was analyzed in the nasopharyngeal carcinoma CNE-2Z cells which over-expressed ClC-3 by pEZ-M03-ClC-3 plasmid transfection. RESULTS: Metformin inhibited the viability of CNE-2Z cells at 5, 10 and 20 mmol/L. Metformin at 10 mmol/L prevented the activation of chloride currents induced by hypotonicity, inhibited the protein expression of ClC-3 chloride channel and arrested the nasopharyngeal carcinoma CNE-2Z cells at G0/G1 phases. ClC-3 chloride channel protein over-expression reversed the effect of metformin on the cell cycle distribution of CNE-2Z cells. CONCLUSION: Metformin inhibits the CNE-2Z cell cycle, which may be related to the inhibition of ClC-3 chloride channel function and protein expression.  相似文献   

3.
AIM: The roles of Cl-channels in regulatory volume decrease (RVD), cell proliferation and cell cycle progression in nasopharyngeal carcinoma cells (CNE-2Z) were investigated. METHODS: Image analysis of living cells was used to detect the volume changes following exposure to hypotonic solutions. Cell viability was determined by the trypan blue assay. MTT method was applied to detected cell proliferation. The effect of the blocker on the cell cycle distribution was monitored by the flow cytometry. RESULTS: 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) inhibited RVD and cell proliferation in a dose-dependent manner. NPPB at the concentration of 100 μmol/L arrested cells in G1 phase (G1 population increased from 54% to 71% at 48 h after treatments), but did not significantly alter cell viability. CONCLUSION: Block of chloride channels suppressed cell proliferation by arresting cells in G1 phase. The results suggest that activation of Cl-channels and RVD is necessary for facilitating cells to proceed to the S phase from G1 phase and maintaining cell proliferation.  相似文献   

4.
AIM: To investigate whether Notch1/Hes1 signaling pathway regulates the expression of CCAAT/enhancer binding protein alpha (C/EBPα), thus affecting the proliferation and differentiation of type Ⅱ alveolar epithelial cells (AECⅡ). METHODS: Human AECⅡ were cultured in vitro, and randomly divided into control group, activator group (adding Notch pathway activator Jagged1 protein, 500 μg/L) and inhibitor group (adding Notch inhibitor DAPT, 10 μmol/L). AECⅡ in each group were collected after 24 h of intervention. The expression of Notch1, Hes1 and C/EBPα at mRNA and protein levels was determined by RT-qPCR and Western blot. The cell proliferation ability of the AECⅡ was measured by living cell counting and CCK-8 assay. The cell cycle distribution and differentiation of the AECⅡ were analyzed by flow cytometry. RESULTS: Compared with control group, the mRNA and protein expression levels of Notch1, Hes1 and C/EBPα were significantly increased in activator group (P<0.05), AECⅡ entered G2/M phase from S phase, the proliferation of AECⅡ was increased, and the differentiation of AECⅡ was reduced (P<0.05). The mRNA and protein expression levels of Notch1, Hes1 and C/EBPα were significantly reduced in inhibitor group (P<0.05), the cell cycle of AECⅡ cells was arrested in G0/G1 phase, the proliferation of AECⅡ cells was reduced, and the differentiation of AECⅡ cells was increased (P<0.05). CONCLUSION: Notch1/Hes1 signaling pathway regulates the expression of C/EBPα and affects the proliferation and differentiation of AECⅡ.  相似文献   

5.
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   

6.
AIM: To investigate the expression of microRNA-141 (miR-141) in human hepatocellular carcinoma (HCC) cell line SMMC-7721 and normal hepatocyte line HL-7702, and to analyze the effect of abnormal expression of miR-141 on the malignant biological behaviors of human hepatocarcinoma cells. METHODS: The RNA from SMMC-7721 cells and HL-7702 cells was extracted. SYBR Green real-time PCR was performed to detect the expression of miR-141. Synthetic miR-141 mimic and its negative control were transfected into the SMMC-7721 cells, and miR-141 inhibitor and its negative control were transfected into the HL-7702 cells by the method of Lipofectamine. After transfection, MTS assay and BrdU-ELISA were employed to evaluate the effect of miR-141 on the cell proliferation. Flow cytometry was used to detect cell cycle and apoptosis. The changes of migration ability were investigated by Transwell invasion assay. RESULTS: The expression of miR-141 in the SMMC-7721 cells was significantly lower than that in the HL-7702 cells (P < 0.05). Compared with blank group, Lipofectamine group and negative control group, the proliferation of the SMMC-7721 cells transfected with 25 nmol/L miR-141 mimic was significantly inhibited in a time-dependent manner (P < 0.05). The percentages of G1 phase cells and early apoptotic rate were significantly increased when miR-141 was up-regulated, but the migration ability was inhibited (P < 0.05). Compared with blank group, Lipofectamine group and negative control group, the proliferation of HL-7702 cells transfected with 50 nmol/L miR-141 inhibitor was significantly increased in a time-dependent manner (P < 0.05). When miR-141 was down-regulated, the percentages of G1 phase cells and early apoptotic rate were significantly decreased, but the migration ability was enhanced (P < 0.05). CONCLUSION: miR-141 is down-regulated in human hepatocarcinoma cell line. Up-regulation of miR-141 will not only inhibit cell proliferation and migration ability, but also affect the cell cycle and apoptosis of SMMC-7721 cells. miR-141 may function as a tumor suppressor gene during HCC development.  相似文献   

7.
AIM:To investigate the effect of Epstain-Barr virus latent membrane protein 1 (EBV-LMP1) on proliferation and cell cycle of nasopharyngeal carcinoma (NPC) cells. METHODS:The expression of EBV-LMP1 was detected by immunohistochemical method (LSAB). Proliferation of NPC cells was identified by MTT method. Cell cycle percentage was detected by flow cytometry analysis. RESULTS: OD value of EBV-LMP1 expressive NPC cells L-CEN1 was much higher than that of both EBV-LMP1 negative NPC cells V-CEN1 and CNE1 (P<0.01). Compared with the cell cycle percentage in both V-CNE1 and CNE1, the percentage of G1 was significantly decreased and the percentage of S was much increased in L-CNE1 (P<0.01). But no obvious differences were observed in all cell cycle percentage between V-CNE1 and CNE1 (P>0.05).CONCLUSION:The expression of EBV-LMP1 on NPC cell might cause some change of cell cycle and enhance cell proliferation.  相似文献   

8.
AIM: To study the effect of curcumin analogues B67 on radioresistant nasopharyngeal carcinoma cells (CNE-2R). METHODS: The effects of B67 on the cell viability and proliferation of CNE-2R and the parent cells CNE-2 were detected by MTT assay and colony formation assay, respectively. The changes of cell cycle, apoptosis and mitochondrial membrane potential were determined by flow cytometry. The morphological changes of the cells were observed under fluorescence microscope. Node mice were subcutaneously inoculated with the cells to determine the tumorigenic ability. RESULTS: The IC50 of B67 on the viability of CNE-2R cells after treatment for 24 h, 48 h and 72 h were 3.96,2.59 and 0.89 μmol/L, respectively, and those of CNE-2 cells were 8.84, 3.55 and 1.10 μmol/L,respectively. The IC50 of B67 on the proliferation of CNE-2R cells after treatment for 48 h was 0.55 μmol/L, and that of CNE-2 cells was 0.73 μmol/L. After treated with B67 for 24 h, CNE-2R and CNE-2 cells at G2/M stage increased from 5.32% to 40.01% and from 9.07% to 15.73%,respectively. After treated with B67 for 48 h, the apoptosis of CNE-2R and CNE-2 cells increased from 5.49% to 38.06% and from 4.99% to 35.74%, respectively. The mitochondrial membrane potential in CNE-2R and CNE-2 cells was decreased by 66.76% and 72.09%, respectively. After treated with B67 for 24 h, the tumorigenic rate of CNE-2R cells was 0%, while the rates of CNE-2 cells in low- and high-concentration groups were 100% and 0%, respectively.CONCLUSION: Curcumin analogue B67 exhibits enhanced suppressive activity on radioresistant nasopharyngeal carcinoma cells by inducing G2/M-phase arrest, promoting cell apoptosis and changing mitochondrial membrane potential.  相似文献   

9.
AIM:To establish SETD2 gene knockout nasopharyngeal carcinoma (NPC) cell strains based on CRIPSR/Cas9 technique and to analyze their proliferation characteristics. METHODS:Sub-quantitative RT-PCR and Western blot were used to detect the expression of SETD2 in immortalized nasopharyngeal epithelial cell line NP-69, well differentiated NPC cell line CNE1, poorly-differentiated NPC cell line CNE2Z and undifferentiated NPC cell line C666-1, and the SETD2 high expression cell line CNE1 was screened. The proliferation ability of CNE1 cells before and after the SETD2 gene knockout was analyzed by CCK-8 and colony formation assay. The cell cycle distribution was detected by flow cytometry, and the expression of cell cycle-related proteins was detected by Western blot. RESULTS:Compared with NP-69 cells, the expression of SETD2 was decreased gradually in CNE1, CNE2Z and C666-1 cells (P<0.01). Based on the CRISPR/Cas9 technique, 2 monoclonal cell strains with SETD2 gene stable knockout, named CNE1-SETD2-KO-#5 and #9, were successfully screened from total 15 monoclones. The results of CCK-8 and plate colony formation assay confirmed that the proliferation ability of CNE1-SETD2-KO-#5 and #9 cells was significantly enhanced compared with CNE1-WT cells (P<0.05). The results of flow cytometry analysis showed that the G1 phase of CNE1-SETD2-KO-#5 and #9 cells was decreased, while the G2/M and S phases were increased significantly (P<0.05). The results of Western blot confirmed the increases in the protein levels of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin B1, cyclin A2, cyclin E1, cyclin-dependent kinases 2 (CDK2) and CDK4, and the decrease in the protein level of p21 after SETD2 gene knockout (P<0.05). CONCLUSION:The NPC cell strains with SETD2 gene knockout were successfully constructed based on CRISPR/Cas9 technique. SETD2 expression correlates with cell differentiation status in the NPC cells. SETD2 gene knockout promotes NPC cell proliferation by up-regulating cyclin D1, cyclin B1, cyclin A2, cyclin E1, CDK2 and CDK4, and down-regulating p21 expression.  相似文献   

10.
AIM: To evaluate the correlation between microRNA-1284 (miR-1284) and gastric cancer, and to investigate the underlying mechanism. METHODS: The expression of miR-1284 was examined by real-time PCR in 63 gastric cancer (GC) tissue samples and 63 non-malignant adjacent tissue samples. The correlation between miR-1284 and the clinicopathological feature of GC was analyzed. Lentiviral vector containing miR-1284 was constructed and transfected into GC SGC-7901 cells. After transfection, the expression of miR-1284 was examined by real-time PCR. The cell activity was evaluated by CCK-8 assay. The cell cycle and apoptosis were determined by flow cytometry. The ability of cell migration was measured by wound-healing assay. The potential target gene of miR-1284 was predicted by online bioinformatic softwares. The expression of JAG1 mRNA was examined by real-time PCR. The protein levels of JAG1, Notch1 and NF-κB were analyzed by Western blotting. RESULTS: Compared with non-malignant adjacent tissue samples, the results of real-time PCR showed significant downregulation of miR-1284 in 42 GC tissue samples (P<0.05). The expression level of miR-1284 was not significantly associated with age and gender of the patients, tumor size, TNM staging and lymph node metastases (P>0.05), but significantly associated with histologic grading (P<0.05). Compared with LV-NC-GFP group and control group, after transfection of miR-1284 in LV-miR-1284 group, the expression of miR-1284 was significantly increased (P<0.05), the percentages of apoptotic cells and the cells in G0/G1 phase were significantly increased (P<0.05), the cells activity and ability of migration were significantly decreased (P<0.05), and the expression of JAG1, Notch1 and NF-κB was significantly decreased (P<0.05). CONCLUSION: The inhibitory effect of miR-1284 on gastric cancer may be associated with the regulation of its targeting gene JAG1.  相似文献   

11.
AIM: To investigate the effect of Ikaros isoforms on the proliferation of human ovarian cancer SKOV3 cells. METHODS: Three isoforms of Ikaros, IK1, IK2 and IK6, were transfected into ovarian cancer SKOV3 cells. CCK-8 assay and cell counting were used to detect the effects of Ikaros isoforms on the proliferation of SKOV3 cells. The cell cycle was analyzed by flow cytometry. The cell cycle-related proteins were detected by Western blot. RESULTS: IK1 and IK2 expression inhibited SKOV3 cells proliferation. Flow cytometry analysis indicated that IK1 and IK2 induced SKOV3 cell cycle arrest at the G1 phase. IK6 isoform exerted no obvious effect on the proliferation or cell cycle of SKOV3 cells. Compared with control EV group, IK1 group and IK2 group showed a dramatic elevation in the expression of the cell cycle inhibitor p21, along with a substantial decrease in the expression of the cell cycle inducers cyclin D1 and cyclin D2, which did not change in IK6 group. CONCLUSION: IK1 and IK2 significantly inhibit the proliferation of ovarian cancer SKOV3 cells and induce cell cycle arrest at G1 phase by regulation of cell cycle-related proteins cyclin D1, cyclin D2 and p21, while IK6 isoform exerts no obvious effect on the proliferation and cell cycle of SKOV3 cells.  相似文献   

12.
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   

13.
AIM: To elucidate the effect of calcitonin gene-related peptide (CCRP) in the therapy of atherosclerosis.METHODS:Effect of CGRP on cell cycle kinetics of cultured vascular smooth muscle cells(HA-VSMC) was investigated by flow cytometry. The expression of cyclins D1 and E required for initiation of S phase were also studied by immunochemistry method. RESULT: CGRP was shown to arrest VSMC in the G0/G1 phase of cell cycle and reduced expression of cyclins D1 and E. CONCLUSION:CGRP inhibits proliferation of HA-VSMC by arresting cells in G1 phase via limiting accumulation of cyclin D1 and E. It might play a role in the therapy of atherosclerosis.  相似文献   

14.
15.
AIM: To observe the inhibitory effects of polypeptide from Buthus martensii venom (PBMV) on human tumor cell lines and the influence of PBMV on cell cycle migration, expression of tumor-suppressor gene p53 and the membrane potential of CNE-2Z cells. METHODS: MTT colorimetric method, the colony formation and mitosis index, flow cytometry assay and intracellular recording with glass microelectrodes were used. RESULTS: PBMV had obvious cytotoxicity on several tumor cell lines. The cells grow was inhibited by PBMV, colony formation rate and mitotic index of tumor cells were reduced and the number of polykaryocyte was decreased. CNE-2Z cells in S phase were reduced evidently after they were treated with PBMV (P<0.01). After CNE-2Z cells were incubated with PBMV, P53 protein expression in the cells decreased obviously. Differences were very distinct (P<0.01). The negative potential of cell membrane reduced evidently and cell membrane was in depolarization state. CONCLUSION: PBMV probably possesses the effects of the "membrane toxin". By decreasing the membrane potential, the growth and proliferation of tumor cells were interfered by PBMV.  相似文献   

16.
AIM: To compare the effects of B50, a mono-carbonyl analogue of curcumin, on the proliferation and apoptosis between homologous nasopharyngeal carcinoma cells CNE-2R and CNE-2 with different radioresistance.METHODS: The effects of B50 on cell viability and cell growth were detected by MTT assay and colony-forming experiment, respectively. The changes of cell cycle, apoptosis and mitochondrial membrane potential (MMP) were determined by flow cytometry.RESULTS: B50 inhibited the cell viability of CNE-2R cells in a time-and dose-dependent manner with the IC50 of (8.06±0.14) μmol/L (24 h), (2.49±0.02)μmol/L (48 h) and (1.42±0.02) μmol/L (72 h), which was more effective than that in CNE-2 cells . The inhibitory effect of B50 on CNE-2R cell growth was more effective than that on CNE-2 cells . After treated with B50 for 48 h, the proportion of CNE-2R cells in G2/M stage was increased from 7.1% to 34.9%, which was better than that of CNE-2 cells (from 12.4% to 35.7%). After treated with B50 for 24 h, the early apoptotic rate in CNE-2R cells was increased from 3.7% to 19.5%, which was better than that in CNE-2 cells (from 4.4% to 14.8%), and the MMP in CNE-2R cells was decreased by (43.17±3.11)%, which was better than that in CNE-2 cells .CONCLUSION: B50 is more effective on inhibiting the cell viability and cell growth, blocking the cell cycle at G2/M stage, inducing apoptosis and decreasing MMP in CNE-2R cells than those in CNE-2 cells, indicating that B50 may enhance the radio-sensitivity of CNE-2R cells by blocking the cell cycle and inducing apoptosis through mitochondrial pathway.  相似文献   

17.
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   

18.
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   

19.
20.
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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