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MiR-202-5p/PTEN mediates doxorubicin-resistance of breast cancer cells via PI3K/Akt signaling pathway

机译:MiR-202-5p / PTEN通过PI3K / Akt信号通路介导乳腺癌细胞对阿霉素的抗性

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摘要

We intended to explore the effect of miR-202-5p and phosphatase and tensin homolog ( ) on doxorubicin (DOX) resistance of breast cancer cells. The result of quantitative reverse transcription-polymerase chain reaction (qRT-PCR) reveals that miR-202-5p was highly expressed in drug-resistant breast cancer tissues, while was expressed less. MiR-202-5p directly targeted . Further, it was found that the overexpression of miR-202-5p promoted the DOX resistance and proliferation as well as decreased apoptosis of MCF-7 cells. The lower expression of miR-202-5p inhibited DOX resistance and proliferation as well as increased the apoptosis of MCF-7/DOX cells. experiments showed that mice with downregulated miR-202-5p had smaller tumor volume and lower Ki67 level. The overexpression of declined the proliferation of MCF7 cells, while miR-202-5p's overexpression could offset the function of overexpression of . The knockdown of promoted MCF7/DOX cell proliferation that could be counteracted by miR-202-5p silence. Moreover, we also revealed that downregulated miR-202-5p expression inhibited PI3k/Akt signaling pathway-related protein by regulating expression of .
机译:我们打算探讨miR-202-5p和磷酸酶以及张力蛋白同系物()对乳腺癌细胞对阿霉素(DOX)耐药性的影响。定量逆转录-聚合酶链反应(qRT-PCR)的结果表明,miR-202-5p在耐药性乳腺癌组织中高表达,而表达却少。直接瞄准MiR-202-5p。此外,发现miR-202-5p的过表达促进了DOX抗性和增殖以及降低了MCF-7细胞的凋亡。 miR-202-5p的较低表达抑制DOX耐药性和增殖,并增加MCF-7 / DOX细胞的凋亡。实验表明,miR-202-5p表达下调的小鼠肿瘤体积较小,而Ki67水平较低。过度表达会降低MCF7细胞的增殖,而miR-202-5p的过度表达可能会抵消MCF7细胞的过度表达。抑制的MCF7 / DOX细胞增殖的抑制作用可能被miR-202-5p沉默所抵消。此外,我们还发现,下调miR-202-5p的表达可通过调节的表达来抑制PI3k / Akt信号通路相关蛋白。

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