首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献，搜索用时 31 毫秒
1.
AIM: To observe the influence of human mutant p27 gene (p27mt) on the growth and so as to investigate the function and mechanism of p27mt in gene therapy for colorectal cancer.METHODS: Colorectal cancer cell line SW480 was infected with recombinant replication defective adenovirus Ad-p27mt,and expression of p27mt protein was detected by Western blotting.The inhibitory effect of p27mt on SW480 and cell cycle were determined by flow cytometry,and DNA fragment was analyzed to identify the occurrence of apoptosis.RESULTS: After transfected with Ad-p27mt,p27 protein was highly expressed in SW480 cells.77.96% colorectal cancer cells were blocked in phase G0/G1,while in Ad-LacZ group and blank control group,27.57% and 25.29% cells were blocked in the same phase,respectively.Growth curve showed Ad-p27mt had an obviously inhibitory effect on the growth of SW480 cells.DNA fragment assay demonstrated that p27mt was able to induce the apoptosis of colorectal cancer cells.CONCLUSION: p27mt has an obvious blocking effect on colorectal cancer cell cycle,and most cells are blocked in phase G0/G1.This blockage is related with the growth inhibition and apoptosis induced by p27mt.  相似文献   

2.
AIM: To investigate the effects of p27kip1 gene on DNA replication and protein synthesis in esophageal carcinoma cells. METHODS: Recombinant adenovirus Ad-p27kip1 was constructed and transfected into esophageal carcinoma cell EC-9706, and its effects on DNA replication, protein synthesis and the growth of esophageal carcinoma cells were explored by means of cell growth count, [3H]-TdR, [3H]-Leucine incorporation method and flow cytometry. RESULTS: The growth of esophageal carcinoma cells was inhibited obviously. The radioactive intensity of -TdR and -Leucine in Ad-p27kip1 group decreased significantly than that in control group after EC-9706 transfection (P<0.01), while the multiplication of esophageal carcinoma cell was inhibited obviously. CONCLUSION: Ad-p27kip1 inhibited the multiplication of the esophageal carcinoma cells, which may be related to its suppressive function for DNA replication and protein synthesis.  相似文献   

3.
AIM: To investigate the promoting effects of survivin-siRNA on apoptosis of DU145 cells. METHODS: The DNA template coding siRNA against survivin was synthesized and recombinant plasmid pSi-sur was constructed. The recombinant and the two controls, liposome and pSi-scrambled plasmid, were transfected into DU145 cells. The expression of survivin in mRNA and protein was detected by RT-PCR and Western blotting, respectively. Apoptosis was measured by acridine orange staining, Annexin V-FITC labeled flow cytometry and TUNEL assay.RESULTS: Compared to the liposome control, the levels of survivin mRNA and protein in siRNA group were 0.28±0.07 and 0.34±0.05 (n=3, P<0.05) respectively 72 h after transfection. The apoptotic rate of the cells in pSi-sur group was significantly higher than that in two control groups as showed in acridine orange staining, Annexin V-FITC labeled flow cytometry and TUNEL assay.CONCLUSION: Survivin siRNA significantly inhibits the expression of survivin both in mRNA and protein levels, and induces apoptosis of DU145 cells in vitro.  相似文献   

4.
AIM:To observe the effect of exogenous androgen responsive element decoy on the promoter of prostate specific antigen (PSA) and the growth of LNCaP cells for searching the possibility of gene therapy for prostate cancer. METHODS:Firstly, pGL3-PSA luciferase expression vector containing 640bp-promoter fragment of PSA gene was constructed. Then, a 23-mer phosphorothioated ARE decoy based on the deduced ARE sequence at the promoter region of PSA gene was synthesized. pGL3-PSA and ARE decoy DNA were cotransfected into PC3-M cell by lipofectamineTM 2000. Through detecting the activity of luciferase, the effect of ARE decoy on the promoter of PSA was studied. Then the ARE decoy DNA was transfected into LNCaP cells. The effect of decoy DNA on the proliferation of LNCaP cells was examined by using MTT assay. The effects of apoptosis were detected by phase contrast microscopy, DNA agrose gel electrophoresis and flow cytometry. Meanwhile, the nuclear extract was prepared from LNCaP cells and DNA-protein interactions were examined by electrophoretic mobility shift assay (EMSA). RESULTS:The reporter assay showed that the activity of luciferase was significantly reduced in the ARE decoy-transfected cells, bnt not in the cells transfected with the control decoy. EMSA demonstrated specific binding of the ARE decoy to androgen receptor. The growth of LNCaP was remarkably inhibited and apoptotic morphological changes as well as DNA fragmentation were observed in the ARE decoy-transfected cells. The rate of apoptosis was 22.4% detected by FCM. CONCLUSION:The ARE decoy is capable of inhibiting the promoter of PSA gene and inducing the apoptosis in prostate cancer cells. It may become a potential therapeutic tool for prostate cancers.  相似文献   

5.
AIM: To study the effect of wild-type p53 gene on the differentiation, apoptosis and expression of scavenger receptor CD36 in U937 cells. METHODS： Recombinant adenovirus vector with wild-type p53 gene was constructed and used to transfect U937 cells. With the expression of wild-type p53 gene following adenoviral infection, transfected U937 cells were largely promoted to differentiate into macrophages. RESUITS： Trypanblue-staining test demonstrated that the percentage of positive cells increased from (14.2±5.5)% to (64.6±9.2)% and nitroblue tetrazolium (NBT) reduction test reached similar results (6.3±1.8)% vs (49.7±12.6)%. Furthermore, CD36 mRNA was up-regulated as confirmed by RT-PCR. The increased expression level of CD 36 was also detected by flow cytometry analysis. CONCLUSION： These results suggest that wild-type p53 gene can affect U937 cells differentiation and apoptosis, up-regulate expression of scavenger receptor CD36. It may have a potential significance on atherogenesis.  相似文献   

6.
AIM: To determine whether triptolide induce apoptosis of synovial cells in collagen-induced arthritis (CIA) in rats. METHODS: The male Wistar rats were used to make CIA models by immunized with Bovine collagen Ⅱ (BCⅡ) in Freund's complete adjuvant (FCA). A total of 20 CIA rats were randomly divided into 2 groups, triptolide group (10 rats) and CIA control group (10 rats). Triptolide group were administered with triptolide at 40 μg/kg body weight intramuscularly every three days. CIA control group and another 10 age-matched normal rats were given normal saline instead. The rats were sacrificed on the 31st day after the triptolide administration. The pieces of synovium of the rat knee joints were harvested. The synovium was examined by HE staining and electron microscope. The apoptosis was tested by TUNEL and flow cytometer. RESULTS: The earlier phase of apoptotic synoviocytes were observed under the electron microscope. The flow cytometry showed that the percentage of the apoptotic cells was (3.98±1.16)% in the triptolide group, (1.83±0.82)% in the CIA control group, and (0.87±0.24)% in the normal group (P<0.01: triptolide vs control group). While the percentage of the cells in DNA synthesis phase was (3.3±1.2)% in the triptolide group, (8.0±1.4)% in the CIA control group, and (3.4±0.7)% in the normal group. There is significantly different in the apoptosis changes between the triptolide group and the CIA control group (P<0.01: triptolide vs CIA control group). The TUNEL labeling demonstrated that the percentage of the apoptotic cells was (4.5±1.0)% in the triptolide group, (2.2±1.0)% in the CIA control group, and (1.0±0.4)% in the normal group. The difference of apoptotic rate between the triptolide group and the CIA control group is significant (P<0.01). CONCLUSION: This study demonstrates that triptolide can induce apoptosis in CIA rats, which may be one of the mechanisms that triptolide treats the rheumatoid arthritis.  相似文献   

7.
AIM: To investigate the apoptosis in primary gastric cancer cells induced by resveratrol, and the relation between this apoptosis and expression of bcl-2 and bax. METHODS: In in vitro experiments, MTT assay was used to determine the cell growth inhibitory rate. Transmission electron microscopy and TUNEL staining were used to quantitatively and qualitively detect the apoptosis of primary gastric cancer cells before and after the resveratrol treatment. Immunohistochemical staining and RT-PCR was used to detect the expression of apoptosis-regulated gene bcl-2 and bax. RESULTS: Resveratrol inhibited the growth of primary gastric cancer cells in a dose- and time-dependent manner. Resveratrol induced primary gastric cancer cells to undergo apoptosis with typically apoptotic characteristics. TUNEL assay showed that after the treatment of primary gastric cancer cells with resveratrol for 24, 48, 72, 96 hours, the apoptotic indexs were 4.93%±0.19%, 16.74%±0.43%, 27.88%±0.36%, 36.84%±1.07% respectively. Immunohistochemical staining showed that after the treatment of primary gastric cancer cells with resveratrol for 24, 48, 72, 96 hours, the positive rates of Bcl-2 proteins were 20.68%±0.49%, 10.84%±0.33%, 6.80%±0.34%, 3.91%±0.15% and the positive rates of Bax proteins were 19.79%±0.98%, 30.74%±0.85%, 40.14%±1.17%, 60.08%±1.64%. After exposed to resveratrol for 24 h, 48 h, 72 h and 96 h, the density of bcl-2 mRNA decreased progressively with elongation of time and the density of bax mRNA increased progressively with elongation of time by RT-PCR. CONCLUSION: Resveratrol is able to induce the apoptosis in primary gastric cancer. This apoptosis may be mediated by down-regulation of Bcl-2 and up-regulation of Bax.  相似文献   

8.
  相似文献   

9.
AIM: To construct a rAAV2-pigment epithelium-derived factor (PEDF) vector and to explore the effect of rAAV2-PEDF on the migration and apoptosis of human retinal capillary endothelial cells (HRCECs). METHODS: PEDF gene was cloned into an adeno-associated virus vector pSNAV. The recombinant pSNAV-PEDF was transfected into BHK cells. The G418 resistant cells were selected and infected with recombinant HSV which packaged the recombinant pSNAV-PEDF. The high-titer rAAV2-PEDF was obtained by purification. After transfected the rAAV2-PEDF into HRCECs, the protein expression of PEDF were detected by Western blotting, the migration of HRCECs was assessed by a boyden chamber, and the apoptosis of HRCECs was analyzed by flow cytometry. RESULTS: The evaluation results of PCR, enzyme digestion, and DNA sequencing showed that the rAAV2-PEDF was constructed correctly. The GFP positive cells were observed under laser scanning confocal microscope 48 h after rAAV2-GFP transfection. The expression level of PEDF protein was higher in experimental group than that in control group. The number of migrated cells was 33.0±2.7 in normal control group, 35.0±3.6 in rAAV2-GFP treatment group, and 12.0±2.1 in rAAV2-PEDF treatment group (P<0.05). In normoxic condition, the apoptotic cells were 2.10%±0.53% in control group, 3.40%±0.62% in rAAV2-GFP group and 1.60%±0.47% in rAAV2-PEDF group (P>0.05). In hypoxic condition, the apoptotic cells were 4.00%±0.55% in CoCl2 treatment group, 6.10%±0.71% in CoCl2+rAAV2-GFP treated group and 40.00%±2.10% in CoCl2+rAAV2-PEDF treatment group (P<0.05). CONCLUSION: rAAV2-PEDF is successfully constructed and PEDF gene is stably expressed in HRCECs after rAAV2-PEDF transfection. Over-expression of PEDF inhibits the migration of HRCECs and induces the cell apoptosis obviously in hypoxia.  相似文献   

10.
AIM:To investigate the effects of Jagged 1 (JAG1) gene silencing on the proliferation and apoptosis of human breast cancer MDA-MB-231 cells. METHODS:The specific recombinant vector pRS-JAG1 was transfected into MDA-MB-231 cells with lipofectamine. The protein expression of JAG1 was observed by Western blotting after transfection. MTT assay was used to detect the effect of JAG1 gene silencing on the growth of the cells. The apoptosis and cell cycle were analyzed by flow cytometry. The protein levels of cyclin D1, p21CIP1/WAF1, p27KIP1, p-Rb, Bcl-2, Bax, Bcl-xL and cleaved caspase-3 were determined by Western blotting. RESULTS:Compared with control group, the expression level of JAG1 was reduced by pRS-JAG1 transfection for 72 h (P<0.05). The growth of MDA-MB-231 cells in shJAG1 group was significantly inhibited (P<0.05). The percentages of G 0/G 1-phase cells and early apoptotic rate were obviously higher in shJAG1 group than those in control group (P<0.05). The shRNA-mediated JAG1 silencing decreased the protein levels of cyclin D1, p-Rb, Bcl-2 and Bax, and increased the protein levels of p21CIP1/WAF1, p27KIP1, Bax and cleaved caspase-3 (P<0.05). CONCLUSION:JAG1 silencing effectively inhibits the proliferation and induces the apoptosis of human breast cancer cells, suggesting that JAG1 might serve as a therapeutic target for triple-negative breast cancer.  相似文献   

11.
AIM:To investigate the inhibitory effect of vector-based RNA interference ( RNAi) on the expression of melanoma associated antigen A3 (MAGEA3) protein in hepatocellular carcinoma cells and on apotposis of hepatocellular carcinoma cells. METHODS:A vector for transcribing specific small hairpin RNA ( shRNA) targeting MAGEA3 gene was constructed ,introduced into hepatocellular carcinoma MEL-ED1 cells by Lipofectamine 2000. The MAGEA3 protein and mRNA expression levels of MEL-ED1 cells were detected by Western blotting and RT-PCR, respectively. The cell apoptosis was studied by DNA fragmentation, electron microscopy ，TUNEL assay, and annexin V/PI staining. RESULTS:The vector of RNA interference was successfully constructed and MAGEA3 expression was descreased significantly in MEL-ED1 cells. After the shRNA expression vector was transfected into the MEL-ED1 cells, the expression of MAGEA3 gene was inhibited significantly ( by 90% ). DNA fragmentation，electron microscopy and TUNEL assay showed classic apoptosis characters in the MEL-ED1 cells transfected with pSilencer-MAGEA3 plasmid with an apoptosis rate of 21.41% ±1.98%, significantly higher than those in the negative control group transfected with pSilencer-neo and in the non-transfected group (both P<0.01). CONCLUSION:The specific small hairpin RNA targeting MAGEA3 mRNA can inhibit the expression of MAGEA3 and cause apoptosis of hepatocellular carcinoma cells , which suggests inhibitory effect of MAGEA3 on apoptosis in cancer and provides an experimental basis for treating human tumors with RNAi.  相似文献   

12.
AIM: To investigate the effect of NKX3.1 on the gene expression of bcl-2 and apoptosis in prostate cancer PC-3 cells. METHODS: The eukaryotic expression plasmid pcDNA3.1- NKX3.1 was transiently transfected into PC-3 cells. RT-PCR and Western blotting were used to detect the effects of NKX3.1 on the expression of bcl-2 gene. Down-regulatory effect of NKX3.1 on bcl-2 gene was detected by EMSA. Flow cytometry and apoptotic body staining were carried out to study the effects of NKX3.1 on apoptosis of PC-3 cells. RESULTS: The mRNA and protein expression of bcl-2 in PC-3 cells was down-regulated by over-expression of NKX3.1. The EMSA result showed that NKX3.1 interacted with the NKX3.1 binding elements in upstream regulatory region of bcl-2 gene. The results of flow cytometry showed that the number of apoptotic PC-3 cells increased by 1.41-fold after NKX3.1 transfection to PC-3 cells. NKX3.1 increased the apoptotic bodies stained by Hoechst 33258 significantly. CONCLUSION: NKX3.1 down-regulates the expression of anti-apoptotic gene bcl-2 and induces the apoptosis of prostate cancer PC-3 cells.  相似文献   

13.
AIM:To investigate the effects of sodium valproate (VPA) on the cell cycle and apoptosis of chronic myeloid leukemia cell line K562, and to explore the possible mechanisms. METHODS:K562 cells were treated with VPA. Cell cycle and apoptosis were analyzed by flow cytometry. The expression of p21WAF1 mRNA was detected by RT-PCR. RESULTS:After treatment with VPA, cell cycle was arrested obviously at G0/G1 phase ［(82.30±9.41)% vs (40.13±2.12)%, P<0.05］. The apoptotic rate was significantly higher in the cells treated with VPA than that in untreated cells ［(11.47%±0.25%) vs (4.77%±0.40%), P<0.05］. The level of p21WAF1 mRNA was increased ［(1.65±0.91) vs (0.25±0.04), P<0.05］. CONCLUSION:VPA induces elevated expression of p21WAF1 mRNA in K562 cells, resulting in G0/G1 phase arrest and apoptosis in vitro.  相似文献   

14.
QI Zhi-lin  LI Lu  WANG Ming  BI Fu-yong 《园艺学报》2010,26(8):1555-1558
AIM: To investigate the enhancing effect of aspirin on the HepG-2 cell apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its underlying mechanism. METHODS: HepG-2 cells were cultured in DMEM medium with 15% fatal bovine serum. Modified carbol fuchsin staining was used to observe the cellular morphology. Cell proliferation was measured by MTT. The method of terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) was used to examine the apoptotic index of the cells. RT-PCR was applied to detect survivin gene expression. The apoptotic rate and cell cycle were determined by flow cytometry. RESULTS: Aspirin at different concentrations and TRAIL inhibited the proliferation of HepG-2 cells and the cell apoptotic index was obviously higher than that in control group. Aspirin increased the apoptotic rate in a dose-dependent manner. Aspirin at different concentrations and TRAIL significantly down-regulated the mRNA level of survivin. CONCLUSION: Aspirin enhances the apoptosis of HepG-2 cells induced by TRAIL and the mechanism may be related to down-regulating the mRNA expression of survivin.  相似文献   

15.
AIM: To study the effect of cellular repressor of E1A-stimulated genes(CREG) and its mechanism on apoptosis of human umbilical vein endothelial cells (HUVECs) induced by etoposide (VP-16).METHODS: Primary HUVECs were cultured. RetroviraI eukaryotic expression vectors pLNCX-CREG and pLXSN-shRNA-CREG were transfected into HUVECs. The stable cell clone was selected and obtained by screening with G418 (800 mg/L) and the puromycin (2.5 mg/L), respectively. CREG expression was detected by Western blotting. The cells with overexpression of CREG (H-C) and those with CREG down-regulation (H-S) were pretreated with apoptotic inducer VP-16 at 100 μmol/L for 6 h. The apoptotic rates of the 3 kinds of cells were analyzed by TUNEL and flow cytometry with annexin V/PI dualstaining. Furthermore, the protein levels of phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) in the 3 kinds of cells were analyzed by Western blotting. The p38-specific inhibitor SB203580(20 μmol/L)was used to investigate the effects of p-p38 expression on apoptosis. RESULTS: Western blotting showed that CREG expression was obviously increased up to 160% in H-C compared to HUVECs. However, CREG expression in H-S cells was identified to be down-regulated to 70% compared with HUVECs. TUNEL assay and annexin V/PI dual-color FACS showed that the apoptotic rate was dramatically increased in H-S cells,but decreased in H-C cells. Subsequently, Western blotting exhibited that p-p38 expression was increased in H-S cells compared to HUVECs and H-C cells. When the H-S was pretreated with SB203580, the apoptotic rate was decreased. CONCLUSION: CREG overexpression might prevent HUVECs from apoptosis by inhibiting p38 MAPK activition.  相似文献   

16.
AIM: To explore the effect of EBV infection on growth and apoptosis of nasopharyngeal carcinoma(NPC) cell line.METHODS: NPC cell line CNE1 was directly infected by Epstein Barr virus (EBV). The expression of EBV-latent membrane protein 1 (EBV-LMP1) and bcl-2 were detected by immunohistochemistry method (LSAB). The growth of NPC cells was identified by MTT method. Apoptotic carcinoma cells were detected by flow cytometry analysis and the terminal deoxynucletidyl transferase-medicated dUTP-biotin nick end labeling (TUNEL) methods. RESULTS: EBV-LMP1 was positive in CNE1 infected by EBV(E-CNE1). Compared with CEN1, the growth of E-CNE1 apparently increased (P＜0.01). No apoptotic carcinoma cells were detected and bcl-2 postive cells were 2%~3% respectively in 2 kinds of NPC cells.CONCLUSION: Growth of NPC cells is enhanced by EBV infection and EBV-LMP1 expression, but no influence on expression of bcl-2 and apoptosis of NPC cells.  相似文献   

17.
AIM: To investigate the effect of microRNA-24-3p (miR-24-3p) on the viability and apoptosis of esophageal cancer cells. METHODS: The expression of miR-24-3p and KLF6 mRNA in the esophageal cancer cells TE11, Eca109 and EC9706 were detected by RT-qPCR. The protein expression of KLF6 was determined by Western blot. EC9706 cells were transfected with anti-miR-24-3p and KLF6 siRNA. The cell viability was measured by MTT assay, the apoptotic rate was analyzed by flow cytometry, and the proliferation, apoptosis and IL-6/STAT3 signaling pathways related proteins were determined by Western blot. The level of IL-6 was measured by ELISA. The dual luciferase reporter gene assay was used to verify the relationship between miR-24-3p and KLF6. RESULTS: The levels of miR-24-3p were up-regulated in the esophageal cancer cells TE11, Eca109 and EC9706 (P < 0.05), and the expression of KLF6 at mRNA and protein levels was down-regulated (P < 0.05). Knock-down of miR-24-3p expression inhibited the cell viability, induced apoptosis, and inhibited the protein levels of CDK4, cyclin D1, CDC25A, p-STAT3, Bcl-2 and IL-6, and promoted the protein expression of caspase-3 and Bax in EC9706 cells. CONCLUSION: miR-24-3p targets KLF6 gene to affect the viability and apoptosis of esophageal cancer cells by regulating IL-6/STAT3 signaling pathway.  相似文献   

18.
AIM:To elucidate the pattern of 5-fluorocytosine(5-FC) induced apoptosis and its role in gene therapy for human pancreatic cancer. METHODS: The human pancreatic cancer SW1990 cells(CEA-producing) were infected with recombinant adenoviruses(Adex1CEA-prCD or Adex1CEA-prZ).Cytosine deaminase(CD) expression was examind by western blot. Apoptosis induced by 5-FC in human pancreatic cancer SW1990 cells genetically modified to express cytosine deaminase was investigated by applying electron microscopy, DNA electrophoresis and flow cytometry analysis techniques. RESULTS: The SW1990 cells infected with Adex1CEA-prCD were treated with 5-FC at 100 μmol·L-1 for 48 h, cell apoptosis occurred. Typical apoptosis morphological feature appeared and DNA ladder could be demonstrated on DNA electrophoresis. Apoptosis peak was also showed by flow cytometry. Apoptotic cells accounted for 34.6% of the cell population. Cells in G1, S and G2/M phase of cell cycle were 64%, 11% and 7%, respectively. CONCLUSION: The apoptosis induced by 5-FC may be a primary mechanism in CD gene therapy for pancreatic cancer.  相似文献   

19.
AIM: To investigate the effect of microRNA-375 (miR-375) on the viability, cell cycle and apoptosis of HCT116 cells.METHODS: The expression of miR-375 in different colorectal cancer cell lines was detected by real-time PCR. The miR-375 mimics was transfected into HCT116 cells by LipofectamineTM 2000. The mRNA expression of miR-375 and AEG-1 was detected by real-time PCR. The HCT116 cell viability was detected by MTT assay. The changes of apoptosis and cell cycle distribution were analyzed by flow cytometry.RESULTS: Real-time PCR showed that miR-375 expression was the lowest in HCT116 among 4 colorectal cancer cell lines. The expression level of miR-375 significantly increased in miR-375 mimics group compared with that in the negative control group. The high expression level of miR-375 significantly inhibited the mRNA expression of AEG-1. After transfection with miR-375 mimics, the cell viability was inhibited, the apoptotic rate was increased, the proportion of G1-stage cells was increased, and the proportion of S-stage cells was decreased.CONCLUSION: miR-375 inhibits the viability, mediates the cell cycle arrest and promotes the apoptosis of colon cancer HCT116 cells. miR-375 may act as a tumor suppressor in colorectal cancer by inhibiting AEG-1.  相似文献   

20.
AIM: To investigate the synergistic effect of p53-inducible gene 7 (PIG7) and histone deacetylase (HDAC) inhibitor valproic acid (VPA) on the differentiation and apoptosis of human leukemia SKNO-1 cells.METHODS: The DNA fragments containing PIG7 open reading frame or antisense oligonucleotides were subcloned into lentiviral vector. SKNO-1 cells were transduced with prepared lentivirus. Transgene expression was detected by semi-quantitative RT-PCR and Western blotting. The expression of myeloid cell differentiation antigen CD11b and the apoptotic cells were analyzed by flow cytometry. DNA fragmentation analysis was also used to observe the apoptosis of SKNO-1 cells.RESULTS: VPA inhibited the proliferation of SKNO-1 cells in a dose-　and time-dependent manner. Compared with control group, the differentiation and apoptosis of SKNO-1 cells were significantly induced by ectopically expressed PIG7 (P<0.05). The apoptosis induced by ectopically expressed PIG7 was further enhanced by VPA treatment (P<0.05), and the typical DNA ladders were also observed. The proportion of CD11b+ SKNO-1 cells notably increased after infection with lentivirus containing PIG7 as compared with empty vector group (P<0.05). Up-regulation of PIG7 also enhanced the susceptibility of the cells to the induction of differentiation by VPA.CONCLUSION: VPA inhibits the proliferation and induces the differentiation and apoptosis of SKNO-1 cells. Enforced expression of PIG7 enhances the differentiation and apoptosis of SKNO-1 cells and promotes the sensitivity of SKNO-1 cells to VPA. Over-expression of PIG7 combined with VPA may provide a new strategy for treatment of leukemia.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号