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首页> 外文期刊>European journal of gynaecological oncology >Silencing S100A4 gene promoted platinum sensitivity in ovarian cancer
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Silencing S100A4 gene promoted platinum sensitivity in ovarian cancer

机译:沉默的S100A4基因促进了卵巢癌的铂敏感性

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摘要

Objective: To explore the relationship of S100A4 and platinum resistance in ovarian cancer. Materials and Methods: S100A4 expression level in tissue slices from 35 cisplatin-sensitive ovarian cancer patients and 28 cispatin-resistant patients were analyzed by immunohistochemistry. Platinum-resistant cells CP70 transfected with S100A4 siRNA were set as experimental group, negative control siRNA, and transfection reagent was also transfected cells and set as negative control group and blank group, respectively. After transfection, S100A4 transcription level of cells was determined by qRT-PCR, the expression levels of S100A4 and PKC/p53 pathway associated proteins were determined by Western-blot; cells 'cisplatin sensitivity and cells' invasion ability were analyzed by MTT method and Transwell assay and the cell cycle and apoptosis was determined by flow cytometry. Results: S100A4 expression level of cisplatinsensitive patients was lower than cisplatin-resistant patients; after transfection, IC50 of blank group, negative control group and experimental group was 75.96, 66.73 and 40.31 mon, respectively; the cells' percentage in G1 phase of experimental group was higher than other groups while in S phase it was lower than other groups (p <0.05); the expression level of PKC-6/8 and p-p53 increased significantly (p < 0.05). Conclusions: Silencing S100A4 gene in CP70 cells could u-regulate the expression of PKC-delta/epsilon and p-p53, thus promoting apoptosis by PKC-delta/epsilon in coordination with p-p53 and increasing chemosensitivity of cells.
机译:目的:探讨S100A4与铂抗性在卵巢癌中的关系。材料和方法:通过免疫组化分析来自35个顺铂敏感的卵巢癌患者的组织切片中的S100A4表达水平。用S100A4 siRNA转染的铂抗性细胞Cp70被设定为实验组,阴性对照siRNA和转染试剂也转染细胞,分别设定为阴性对照组和空白组。转染后,通过QRT-PCR测定细胞的S100A4转录水平,通过蛋白质印迹测定S100A4和PKC / P53途径相关蛋白的表达水平;通过MTT方法分析细胞'顺铂敏感性和细胞的侵袭能力,并通过流式细胞术测定细胞周期和细胞周期和细胞凋亡。结果:S100A4顺铂患者的表达水平低于顺铂耐药患者;经过转染后,空白组的IC50,阴性对照组和实验组分别为75.96,66.73和40.31个周一;实验组G1阶段的细胞的百分比高于其他组,而在S期间低于其他基团(P <0.05); PKC-6/8和P-P53的表达水平显着增加(P <0.05)。结论:CP70细胞中的S100A4基因可以调节PKC-DELTA / EPSILON和P53的表达,从而通过PKC-DELTA / EPSILON与P-P53的协调促进细胞凋亡并增加细胞的化学敏感性。

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