共查询到20条相似文献，搜索用时 31 毫秒
1.
AIM: To down-regulate expression of c-myc through antisense therapy and to investigate its effect on the sensitivity of osteosarcoma MG-63 cells to cisplatin-induced apoptosis. METHODS: The recombinant adenovirus (Ad-Asc-myc) encoding antisense c-myc fragment was constructed and transfected into osteosarcoma MG-63 cells in vitro in order to down-regulate the expression of c-myc, and the change in the sensitivity to cisplatin-induced apoptosis was observed. MTT, Western blot, RT-PCR, flow cytometry (FCM) and electron microscope were used to evaluate tumor cell proliferation in vitro, genes expression related to apoptosis regulation and effects on the sensitivity of osteosarcoma MG-63 cells to cisplatin-induced apoptosis. RESULTS: Ad-Asc-myc down-regulated the expression of c-myc protein after transfected MG-63 cells for 48 h, combined with the treatment of 2.0 mg/L cisplatin for 2 h inhibited tumor cell proliferation in vitro by 38.0%. RT-PCR revealed that Ad-Asc-myc down-regulated the expression of Bcl-2 and up-regulated the expression of Bax. No appreciable change was observed in the expression of E2F-1. FCM showed that Ad-Asc-myc induced apoptosis in intransfected cells, and rendered it more sensitive to cisplatin. CONCLUSION: Antisense c-myc is able per se to induce apoptosis and sensitize osteosarcoma cells to cisplatin-induced apoptosis. 相似文献
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AIM: The cancer biology has showed that overexpression of oncogenes is responsible for the progression of human malignancies,antisense technology can block a certain gene expression.Caffeine has enhancement effect on chemotherapy of osteosarcoma cells to cisplatin,we constructed the recombinant adenovirus (Ad-Asc-myc) encoding antisense c-myc fragment and investigated its effect on the in vitro sensitivity of osteosarcoma MG-63 cells to cisplatin.METHODS: The recombinant adenovirus (Ad-Asc-myc) encoding antisense c-myc fragment was constructed by cloning c-myc cDNA of about 750 base pairs in a reverse direction into adenovirus vector.Ad-Asc-myc and caffeine was used respectively or together to co-operate with cisplatin to treat the osteosarcoma MG-63 cells in vitro,and Western blotting,MTT,flow cytometry (FCM),electron microscope were used to evaluate expression of c-Myc protein,tumor cell proliferation in vitro,apoptosis and cell cycle analysis.RESULTS: Ad-Asc-myc was obtained with the titer of 2×1012 pfu/L.Ad-Asc-myc down-regulated the expression of c-Myc protein,Ad-Asc-myc or caffeine enhanced the effects of 2.0,5.0 mg/L cisplatin on MG-63 cells.Moreover,Ad-Asc-myc combined with caffeine significantly enhanced this effects,not only on cisplatin-induced apoptosis,but also on tumor cells proliferation in vitro.The expression of bcl-2 was downregulated,bax were upregulated,while there was no change in the expression of E2F-1.FCM analysis showed that cisplatin treatment induced a block in S phase,and caffeine reversed this block and speeded up the progression of cells out of the S phase.Ad-Asc-myc induced obvious G2/M phase arrest in transfected cells.CONCLUSION: Ad-Asc-myc combined with caffeine may enhance apoptosis-induced and chemotherapy effects of osteosarcoma MG-63 cells to cisplatin. 相似文献
3.
AIM: To detect the expression of miRNA-363 and SOX4 in osteosarcoma tissues and to investigate the effect of miRNA-363 on the viability and apoptosis of human osteosarcoma cell line MG-63.METHODS: Real-time PCR was used to detect the expression level and the relationship of miRNA-363 and SOX4 mRNA in the osteosarcoma tissues and the corresponding paratumorous tissues collected from 63 patients. The expression levels of miRNA-363 and SOX4 in osteosarcoma cell line MG-63 after transfected with miRNA-363 mimics were measured. The cell viability was measured by CCK-8 assay. Flow cytometry was used to monitor the changes of cell cycle and apoptosis. The changes of SOX4 and miRNA-363 expression levels in the MG-63 cells after transfection with SOX4 siRNA or pcDNA/SOX4 was detect by real-time PCR.RESULTS: The expressed level of miRNA-363 was lower, and the expression level of SOX4 was higher in the osteosarcoma tissues than those in the adjacent normal tissues. A significantly negative correlation between the expression levels of miRNA-363 and SOX4 was observed. The expression of miRNA-363 in the MG-63 cells after transfection with miRNA-363 mimics was significantly up-regulated, while the expression of SOX4 in the MG-63 cells was significantly down-regulated, with significant difference as compared with the cells transfected with miRNA-NC and control cells. The viability of MG-63 cells was inhibited, the cell cycle was arrested in G0/G1 phase, and the cell apoptosis was increased by transfection with miRNA-363 mimics. The relative protein expression levels of SOX4 in SOX4 siRNA group and pcNDA/SOX4 group were significantly different from those in negative control group, but the relative expression levels of miRNA-363 had no significant difference. Over-expression of SOX4 restored the viability of the MG-63 cells reduced by miR-363.CONCLUSION: The expression level of miRNA-363 is low in human osteosarcoma tissue. miRNA-363 may inhibits the viability of osteosarcoma cell line MG-63 and promotes cell apoptosis in vitro via inhibiting the SOX4 expression. 相似文献
4.
WANG Li-min 《园艺学报》2015,31(9):1715-1719
AIM: To investigate the effect of Ginsenoside Rh2(Rh2) on the apoptosis of human osteosarcoma cell line MG-63.METHODS: The cell viability was determined by MTT assay. MG-63 cell apoptotic rate was examined by flow cytometry with Annexin V-PI double staining. The expression of Bcl-2, Bax, cytochrome C(Cyt C) and cleaved caspase-3 were measured by Western blot.RESULTS: Rh2 enhanced the apoptosis of MG-63 cells in a dose-dependent manner. Furthermore, after treatment with Rh2, the release of mitochondrial Cyt C and Bax expression were increased, while Bcl-2 and the ratio of Bcl-2/Bax were decreased as compared with control group(P<0.05). The protein level of cleaved caspase-3 was also increased(P<0.05).CONCLUSION: Ginsenoside Rh2 accelerates the apoptosis of MG-63 cells through mitochondria-dependent pathway, suggesting that Rh2 is a novel approach for the treatment of osteosarcoma. 相似文献
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6.
AIM: To investigate the effects of resveratrol on the viability, invasion and autophagy of osteosarcoma MG-63 cells and the regulatory effect of microRNA-34a (miR-34a). METHODS: MG-63 cells were divided into 6 groups:control group and resveratrol treatment groups at doses of 10, 20, 40, 60 and 80 μmol/L. MTT assay, Transwell chamber method and Western blot were used to detect the effects of resveratrol on the viability, invasion ability and expression of autophagy-related proteins in the osteosarcoma cells. The effect of resveratrol at different concentrations on the expression of miR-34a in the osteosarcoma cells was detected by RT-qPCR. The effects of miR-34a mimic and miR-34a mimic negative control (miR-34a NC) transfection on the viability and invasion ability of osteosarcoma cells after treated with resveratrol at different concentrations were analyzed. The effects of miR-34a mimic transfection on autophagy-related proteins LC3-I, LC3-Ⅱ and beclin-1 were determined by Western blot. RESULTS: Compared with control group, resveratrol inhibited the viability and invasion ability of the MG-63 cells and promoted autophagy (P<0.05). Resveratrol up-regulated the expression of miR-34a in the MG-63 cells in a dose-dependent manner (P<0.05). In addition, the ratio of LC3-Ⅱ/LC3-I was increased, and beclin-1 was up-regulated (P<0.05). Co-treatment with miR-34a mimic and resveratrol increased inhibitory effects of resveratrol on the viability and invasion ability and invasion of the MG-63 cells and also promoted autophagy. CONCLUSION: Resveratrol inhibits the viability and invasion of osteosarcoma MG-63 cells and promotes auto-phagy by up-regulating miR-34a expression. 相似文献
7.
AIM:To investigate the suppressive effects of dehydroepiandrosterone (DHEA) and glucose-6-phosphate dehydrogenase (G6PD) antisense oligodeoxynucleotides on Raji cells. METHODS:Raji cell line was cultured in vitro in the presence of DHEA at different concentrations ranged from 0.05 μmol/L to 500 μmol/L or G6PD antisense oligodeoxynucleotides. The viability and proliferation of the cells pretreated with dehydroepiandrosterone or G6PD antisense oligodeoxynucleotides were evaluated. Meanwhile, intracellular activities and mRNA expression of G6PD were analyzed. RESULTS:DHEA and G6PD antisense oligodeoxynucleotides does not influence the viability of cells in culture. Raji cells treated with DHEA at concentration of 50 μmol/L or 500 μmol/L for 72 h or with 10.0 μmol/L G6PD antisense oligodeoxynucleotides for 48 h had significant lower cell numbers compared with control (P<0.01). Raji cells treated with DHEA at concentration more than 5.0 μmol/L for 72 h had significant decreased G6PD activities (P<0.01) but no change in mRNA expression levels was observed. With 10.0 μmol/L G6PD antisense oligodeoxynucleotides pretreatment for 48 h, the G6PD mRNA expression levels and activities were significantly decreased (P<0.01). CONCLUSION:DHEA or G6PD antisense oligodeoxynucleotides at specific concentration have suppressive effects on G6PD activities and proliferation in Raji cells to a certain extent, but the suppressive mechanisms are different. 相似文献
8.
AIM:To investigate the synergistic effect of resveratrol and 5-fluorouracil on osteosarcoma CD133+ cell subset.METHODS:Human osteosarcoma cell line MG-63 CD133+ cell subset and the corresponding CD133- cell subset were treated with resveratrol and 5-fluorouracil.After treatment,the viability of MG-63 cells was measured by MTT assay.The apoptosis of MG-63 cells was analyzed by flow cytometry.Activation of caspase-9 and caspase-3,the expression of Apaf-1,and the release of cytochrome C were evaluated by Western blot.The interaction between Apaf-1 and pro-caspase-9 was detected by co-immunoprecipitation.RESULTS:The cell death and apoptosis of MG-63 CD133+ cell subset induced by 5-fluorouracil were significantly weaker than those in the corresponding MG-63 CD133- cell subset.However,co-treatment with resveratrol significantly enhanced the effect of 5-fluorouracil on inhibiting the viability of MG-63 CD133+ cell subset.Mechanically,treatment with resveratrol upregulated the expression of Apaf-1.Transfection with Apaf-1 siRNA abolished the synergistic effect of resveratrol and 5-fluorouracil in MG-63 CD133+ cell subset.In addition,the results of co-immunoprecipitation indicated that the combination of resveratrol and 5-fluorouracil significantly induced the formation of Apaf-1/pro-caspase-9 complex,leading to the activation of caspase-9 in MG-63 CD133+ cell subset.CONCLUSION:Resveratrol enhances 5-fluorouracil-induced apoptosis of osteosarcoma CD133+ cell subset by promoting the formation of Apaf-1/caspase-9 complex. 相似文献
9.
AIM: To observe the antiproliferative effect of c-myc antisense oligonucleotide in rat thymus lymphocytes. METHODS: Rat thymus lymphocytes were separated by Ficoll-Urografin density gradient centrifugation. Lipofectin was used to introduce antisense, sense and mismatched oligonucleotides for c-myc to rat thymus lymphocytes. The antiproliferative effect was assayed by incorporation of [3H]-TdR and MTS cell proliferation assay. TR-PCR was used to detect the expression of c-myc mRNA. RESULTS: c-myc antisense oligonucleotide inhibited ratthymus lymphocytes proliferation[(0.14±0.03)A vs(0.32±0.16)A,P<0.05],but this ef ect had no relationship with the concentration of c-myc antisense oligonucleot ide.c-myc antisense oligonucleotide decreased the expression of c-myc mRNA in rat thymus lymphocytes. CONCLUSION: c-myc antisense oligonucleotide inhibited rat thymus lymphocyte proliferation. 相似文献
10.
AIM: To explore the inhibitory effect of anti-miRNA-21 oligonucleotide (AMO-miRNA-21) on human leukemic K562 cells. METHODS: K562 cells were transfected with AMO-miRNA-21, which was complementary to the miRNA-21 in a sequence-specific manner. Viability of K562 cells was measured by MTT assay and the optimal concentration for transfection was determined. The inhibitory effect of AMO on the K562 cell growth was examined by trypan blue dye exclusion assay at 24 h, 48 h and 72 h after transfection. Giemsas staining was used to detect morphologic changes of the transfected cells. The cell apoptosis and cell cycle progression were assayed by flow cytometry. Expression of microRNA-21 in the cells was measured by real-time PCR. RESULTS: The growth of cells treated with AMO-miRNA-21 was obviously inhibited compared with that in control groups (P<0.05). Very low cytotoxic and high inhibitory effects of AMO-miRNA-21 were found at concentration of 0.6 μmol/L. The inhibitory effect lasted for 72 h. Apoptotic cells were increased in AMO group and typical morphologic changes were conformed by Giemsas staining. One visible hypodiploid peak was detected in the histogram. However, the cell cycle progression was not inhibited evidently. The expression of microRNA-21 in the transfected cells was down-regulated significantly. CONCLUSION: Targeted inhibition of microRNA-21 with antisense oligonucleotide effectively suppresses leukemic K562 cells growth by inducing apoptosis. miRNA-21 might be a potential target for leukemia therapy. 相似文献
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AIM:To observe the expression of long noncoding RNA TTTY15 in osteosarcoma tissues and cell lines and to explore its effect on the viability and invasion ability of osteosarcoma cell lines. METHODS:qPCR was used to detect the expression of TTTY15 in 11 cases of osteosarcoma and its adjacent tissues. The mRNA levels of TTTY15 in osteosarcoma cell lines (143B, Saos2, MG-63, U2OS and HOS) and human osteoblast cell line hFOB1.19 were also tested. TTTY15 was down-regulated after transfected with small interfering RNA in MG-63 cells, the cell line with the highest level of TTTY15. The effect of TTTY15 knockdown on the viability of MG-63 cells was measured by CCK-8 assay. The cell cycle distribution was analyzed by flow cytometry. The effect of TTTY15 knockdown on the cell invasion ability was detected by Transwell assay. The levels of miR-216b-5p and FOXM1 mRNA were detected by qPCR, and the changes of the related proteins were determined by Western blot. RESULTS:Compared with the adjacent tissues, the expression of TTTY15 increased in the osteosarcoma tissues (P<0.01). Compared with the human osteoblast cell line, the expression of TTTY15 increased in the osteosarcoma cell lines (P<0.05), and the level of TTTY15 in the MG-63 cells was the highest (P<0.01). After knockdown of TTTY15 expression in the MG-63 cells, the cell viability was decreased (P<0.05), cell cycle progression was inhibited (P<0.01), and the cell invasion ability was decreased (P<0.01). The expression of miR-216b-5p was increased (P<0.01) and the expression of FOXM1 mRNA was decreased (P<0.01). The protein expression of FOXM1, CDK4, cyclin D1, MMP-2 and N-cadherin was decreased, while the protein expression of E-cadherin was increased (P<0.05). CONCLUSION:The expression of TTTY15 is increased in the osteosarcoma tissues and cell lines. The low expression of TTTY15 inhibits the cell viability and invasion ability of osteosarcoma cells. The possible mechanism is that the knockdown of TTTY15 expression results in the increase in miR-216b-5p expression and the down-regulation of FOXM1 expression. 相似文献
12.
YANG Lei ZHANG Lian-ying CHEN Wei-wen HU Xiao-yan ZHANG Jian-ye CUI Fu-ai 《园艺学报》2006,22(11):2194-2197
AIM:To observe the effect of curcumin on the proliferation and apoptosis of prostate cancer cell line LNCap. METHODS:LNCap cells were treated with different doses (10 μmol/L, 20 μmol/L, 30 μmol/L, 40 μmol/L) of curcumin and its effects were analyzed in cell growth and apoptosis by microscope, MTT colorimetric assay and flow cytometry. The expression of prostate specific antigen (PSA) was measured by AXSYMTM system-chemical luciferase methods and expression of androgen receptor (AR) was detected by Western blotting. RESULTS:The results showed that curcumin inhibited the proliferation of LNCap cells. The cell growth was inhibited by curcumin in a dose dependent manner and the optimal dose and time was 40 μmol/L, 24 h. Curcumin induced apoptosis in LNCap cells, the most dramatic dose was 40 μmol/L curcumin, at this dose the apoptosis rate was 9.23%. Curcumin inhibited the expression of PSA in LNCap cells and the most dramatic dose and time was 40 μmol/L, 24 h. The PSA in this group was 20% of the control group. Curcumin inhibited the expression of AR on prostate cancer cells. CONCLUSION:Curcumin decreases proliferation and induces apoptosis in LNCap cells in a dose-dependent manner. Curcumin also inhibites the expression of PSA and AR on LNCap cells. 相似文献
13.
AIM：To investigate the regulatory role of miR-335 on the proliferation of human osteosarcoma cell line MG-63. METHODS：Luciferase reporter gene assay was used to detect the specific binding ability of miR-335 to Sp1 3’-untranslated region (UTR). Real-time PCR and Western blotting were used to evaluate the expression of Sp1 mRNA and protein, respectively. MTT assay was used to analyze the proliferation of MG-63 cells. RESULTS：The luciferase reporter gene assay showed that miR-335 targeted Sp1 3’-UTR. Western blotting and real-time PCR showed that miR-335 inhibited the protein expression of Sp1, but had no effect on the mRNA expression of Sp1. Transfection of Sp1 expression plasmid increased the protein and mRNA expression of Sp1. MTT assay showed the viability of MG-63 cells transfected with miR-335 was significantly decreased compared with negative control. Transfection of Sp1 expression plasmid partly reversed the inhibitory effect of miR-335 on the proliferation of MG-63 cells. CONCLUSION: miR-335 inhibits the proliferation of human osteosarcoma MG-63 cells, which may be related to its targeting on Sp1 3’-UTR and the subsequent down-regulation of Sp1 expression. 相似文献
14.
AIM: To study the effects of arsenic trioxide (As2O3) on mouse airway fibroblast (FB) proliferation and expression of c-myc and c-sis in cultured FB. METHODS: The cultured FB was divided into seven groups. NS, dexamethasone (1.0 μmol/L) and As2O3 at concentrations of 0.25, 0.5, 1.0, 2.0, 4.0 μmol/L were instilled respectively into cultured FB. The effects of different concentration of As2O3 and dexamethasone on cell growth were observed at 1, 3, 5 and 7 day. The changes of cell cycle and the positive expression rate of c-myc and c-sis were examined by flow cytometry (FCM). RESULTS: Various concentrations of As2O3 significantly inhibited the proliferation of FB in vitro and showed a dose-dependent and time-dependent tendency. Data from FCM indicated that G1-phase cell percentage increased and G2/M-phase cell percentage decreased with the increase in As2O3 concentrations. The expression of c-myc and c-sis was significantly inhibited by As2O3 (2.0, 4.0 μmol/L). CONCLUSION: As2O3 inhibits FB proliferation by downregulating the expression of c-myc and c-sis. 相似文献
15.
AIM: The effects of selenium dioxide (SeO2) on proliferation, apoptosis, intracellular reactive oxygen species (ROS) and Ca2+ levels in three leukemia cell lines NB4, K562 and HL-60 were investigated. METHODS: Three leukemia cell lines were treated with 3-30 μmol/L SeO2. Flow cytometry was used to detect apoptosis rate, and analyze the changes of ROS and Ca2+ level within cells. RESULTS: SeO2 at 10 and 30 μmol/L inhibited proliferation in three leukemia cell lines. Treatment with 30 μmol/L SeO2 for 48 h induced 54.0%, 46.5%, 49.6% apoptosis in NB4, K562, and HL-60 cells, respectively, and also markedly decreased ROS and Ca2+ levels among three cell lines. The rate of ROS positive cells in NB4 and HL-60 decreased with the increase in SeO2 concentrations. ROS was clearly reduced with 30 μmol/L SeO2 in K562. Ca2+ levels were tardily declined with 10, 30 μmol/L SeO2 in NB4 and HL-60 cells. Ca2+ levels were clearly reduced with 30 μmol/L SeO2 in K562. CONCLUSION: SeO2 induces apoptosis in three leukemia cells. The declines of intracellular ROS and Ca2+ levels are involved in apoptosis induced by SeO2. 相似文献
16.
AIM: To investigate the effects of baicalin on proliferation inhibition and apoptosis induction in human Burkitt lymphoma cell line CA46 and to explore its underlying mechanisms. METHODS: CA46 cells were exposed to baicalin at different dosages and its proliferation inhibition was detected by MTT assay. The ability of baicalin to induce CA46 cell apoptosis was examined by Annexin V-FITC/PI double staining analysis, TUNEL labeling method and DNA fragmentation. The mRNA expressions of c-myc and bcl-2 were detected by RT-PCR, and the protein expressions of c-Myc, Bcl-2, caspase-3 precursor (procaspase-3) and poly ADP-ribose polymerase (PARP) were detected by Western blotting. RESULTS: Baicalin remarkably inhibited the CA46 cell proliferation, with an IC50 value of 10 μmol/L. Apoptosis was remarkably induced by baicalin in a dose-dependent manner, and its earlier and later stages were detected by annexin V-FITC/PI double staining analysis, TUNEL labeling method and DNA fragmentation, respectively. Furthermore, RT-PCR showed that the mRNA expressions of c-myc and bcl-2 in treated CA46 cells decreased in a time-dependent manner. Western blotting showed that the protein expressions of c-Myc, Bcl-2, procaspase-3 and PARP (116 kD) in baicalin treated CA46 cells were down-regulated in a time-dependent manner, while the expression of PARP(85 kD) was up-regulated. CONCLUSION: Baicalin efficiently induces proliferation inhibition and apoptosis in CA46 cells, which may be related with the down-regulation of c-Myc and Bcl-2 expressions, as well as the up-regulation of caspase-3 activity. 相似文献
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AIM: To study the role of c-myc oncogene in L6565 leukemia oncogenesis and the effects of therapy by inhibition of its expression with antisense c-myc. METHODS: A recombinant retroviral vector containing antisense c-myc of the murine (pGNCas) was constructed and then transfected into PA317 cells by the method of calcium phosphate precipitation. L6565 clone cells were infected with retrovirus particles. Stable integretion of antisense c-myc was shown by PCR. The change of the malignance and phenotype of L6565as were detected by the examination of the growth, morphology, cells cycle, agar assay and expression of c-myc. RESULTS: The shape of most L6565as cells became spherical. The growth of L6565as was inhibited compared to control cells. The analysis of cells cycle: L6565as cells were arrest in G0/G1 phase, decreased in S phase. The ability of L6565as cells to form colony in soft agarose was significantly suppressed. c-myc in L6565as cells was lowly expressed. CONCLUSION: (1)c-myc plays a critical role in L6565 leukemia oncogenesis; (2)Inhibition of expression of c-myc makes partly reversion of malignant phenotype of L6565 murine leukemia clone cells. 相似文献
18.
AIM: To investigate whether antisense oligodeoxynucleotides of hTERT、bcl-2 and c-myc could enhance the sensitivity of leukemia cell K562 to cisplatin. METHODS: The inhibiting effects of cisplatin and cisplatin plus antisense oligodeoxynucleotide on K562 cells were determined by MTT. RESULTS: The inhibiting rate of 20 μmol/L cisplatin to K562 cell is 17.17%±1.36% and it becomes 25.41%±1.77%, 26.18%±1.43% and 28.29%±1.05%, respectively, as combinated with antisense oligodeoxynucleotide of hTERT, bcl-2 or c-myc. CONCLUSION: These results indicated that antisense oligodeoxynucleotides of hTERT, bcl-2 and c-myc enhanced efficacy of cisplatin in K562 leukemic cells. 相似文献
19.
AIM: In this study, we investigated the anticancer effect and mechanisms of manumycin on pancreatic cancer cell line-Panc-1 and the role of p38MAPK pathway in apoptosis. METHODS: The test of anticancer effect was performed by MTT assay. Apoptosis was induced in the cells by manumycin and then treated with SB203580, a specific p38MAPK inhibitor. A quantitative caspase-3 activity assay kit was used in this experiment. RESULTS: Manumycin (6 μmol/L, 18 μmol/L, 54 μmol/L) significantly inhibited cell growth of pancreatic cancer cell line Panc-1. The inhibition rates 24 h after treatment with 6 μmol/L, 18 μmol/L and 54 μmol/L manumycin were 8.9%, 21.9% and 67.0%, respectively. Compared with the control group, the survival levels of the last two groups were of significant statistical difference (P<0.01). The anticancer effects also showed dosage-effect relationship, the value of IC50 24 h after treatment was 34.7 μmol/L. In addition, this reagent simultaneously activated caspase-3 protein, which was partly blocked by p38MAPK specific inhibitor, SB203580. CONCLUSION: Manumycin exerted anticancer effect on Panc-1 cell line via inducing cell apoptosis, which was partly regulated by p38MAPK. 相似文献
20.
AIM: To investigate the effect of chloride channel CLCN2 antisense oligonucleotide on the cell injury of malignant U251 glioma cells induced by cisplatin (DDP). METHODS: The experiment was divided into 4 groups: control group (nonsense oligonucleotide), CLCN2 antisense oligonucleotide group, DDP group (DDP＋nonsense oligonucleotide), DDP＋CLCN2 antisense oligonucleotide group. The viability of U251 cells was measured by MTT assay, CLCN2 mRNA level was determined by RT-PCR, cell apoptosis was measured by TUNEL assay. RESULTS: Compared to the control group, the cell viability, CLCN2 and cyclinD1 mRNA decreased in CLCN2 antisense oligonucleotide group, DDP treated group and CLCN2 antisense oligonucleotide with DDP treated group, cells apoptosis increased. Compared to DDP group, the cell viability (P<0.05) and CLCN2 mRNA decreased in CLCN2 antisense oligonucleotide with DDP treated group, and cells apoptosis increased (P<0.01). Compared to CLCN2 antisense oligonucleotide group, CLCN2 mRNA significantly decreased (P<0.01) in CLCN2 antisense oligonucleotide with DDP treated group. CONCLUSION: CLCN2 antisense oligonucleotide inhibits the expression of CLCN2 mRNA in U251 cells. Inhibition of CLCN2 mRNA facilitates the cell injury of U251 cells induced by DDP. The decrease in CLCN2 mRNA is involved in the mechanism of cell injury by DDP. 相似文献