Effects of RNPC1 gene chemosensitivity of human breast cancer cells SUM1315
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    Abstract:

    Objective:To investigate the effects of RNPC1 gene on chemosensitivity of human breast cancer cells SUM1315 and correlated mechanism. Methods:Lentivirus was used to over-express and knock-down RNPC1 in the SUM1315 breast cancer cells. The cells were divided into overexpress RNPC1(RNPC1)group and its control(NC group),knock-down RNPC1(shRNPC1 group)and its control(SCR group). Real-time PCR and Western blot were analyzed the mRNA and protein expression of RNPC1 in SUN1315 cells. The effect of RNPC1 gene on the sensitivity of the chemotherapeuties drug such as paclitaxel,Taxotere and 5-Fluorouracil with different concentration was detected by CCK8. Apoptosis of breast cancer cell after treated with paclitaxel,Taxotere and 5-Fluorouracil were analyzed by flow cytometry. Results:The qRT-PCR and Western blot results showed that the mRNA and protein level of RNPC1 was increased after transfection with RNPC1 overexpression(RNPC1). While,RNPC1 was reduced after transfection with RNPC1 knock-down RNPC1(shRNPC1)lentivirus. After treatment with different concentration of paclitaxel,Taxotere and 5-Fluorouracil,the IC50 of shRNPC1 group was significantly lower than SCR group(P < 0.05). Furthermore,the IC50 of RNPC1 group was significantly higher than NC group(P < 0.05).The flow cytometer assay was used after treatment with paclitaxel,Taxotere and 5-Fluorouracil for 72 h in the experimental groups. The cell apoptosis rate of shRNPC1 group was higher than SCR group,while,the cell apoptosis rate of RNPC1 was lower than NC group. Conclusions:RNPC1 gene can effectively decrease the sensitivity of human breast cancer cells SUM1315 to the chemotherapeutics drug such as paclitaxel,Taxotere and 5-fluorouracil,indicating that RNPC1 gene silencing might be considered as a new therapeutic strategy for breast cancer.

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薛金秋,石 靓,丁 强. RNPC1基因对人乳腺癌细胞SUM1315化疗药物敏感性的影响[J].南京医科大学学报(自然科学版英文版),2019,(5):648-652.

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  • Received:October 11,2018
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  • Online: May 31,2019
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