首页> 外文期刊>Artificial cells, nanomedicine, and biotechnology. >The circular RNA hsa-circ-0072309 plays anti-tumour roles by sponging miR-100 through the deactivation of PI3K/AKT and mTOR pathways in the renal carcinoma cell lines
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The circular RNA hsa-circ-0072309 plays anti-tumour roles by sponging miR-100 through the deactivation of PI3K/AKT and mTOR pathways in the renal carcinoma cell lines

机译:环状RNA hsa-circ-0072309通过灭活PI3K / AKT和mTOR通路在肾癌细胞系中海绵化miR-100而发挥抗肿瘤作用

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Aims: To explore the roles and regulatory mechanisms of the circular RNA (circRNA)-hsa-circ-0072309 in CAKI-1 and ACHN cells. Methods: CAKI-1 and ACHN cells were transfected with hsa-circ-0072309 overproduction vector (circRNA) and microRNA-100 (miR-100) mimic or the corresponding controls. Cell viability was detected with the CCK-8. The protein expression levels of p53, c-Myc, cleaved-caspase-3/9, matrix metalloproteinase (MMP)-2/9, vimentin, AKT, PI3K and mTOR were individually determined through western blot. qRT-PCR was used to examine the expressions of hsa-circ-0072309 and miR-100. The apoptotic rate and the migration or invasion rates were separately determined by the annexin v-FITC/PI with a flow cytometer and modified two-chamber migration assay or millicell hanging cell culture. Results: The hsa-circ-0072309 was poorly expressed in tumor tissue. Abundant hsa-circ-0072309 induced the inhibitions of cell proliferation, migration and invasion, as well as the PI3K/AKT and the mTOR cascades but enhancement of apoptosis. circRNA stimulated the down-regulation of miR-100, which was low-expressed in tumour tissue and whose overproduction abolished the impacts of circRNA on these elements mentioned above. Conclusion: The hsa-circ-0072309 played anti-tumour roles by targeting miR-100 by blocking the PI3K/AKT and mTOR cascades in the CAKI-1 and ACHN cell lines.
机译:目的:探讨环状RNA(circRNA)-hsa-circ-0072309在CAKI-1和ACHN细胞中的作用和调控机制。方法:用hsa-circ-0072309过量生产载体(circRNA)和microRNA-100(miR-100)模拟物或相应的对照转染CAKI-1和ACHN细胞。用CCK-8检测细胞活力。通过蛋白质印迹分别测定了p53,c-Myc,裂解半胱氨酸蛋白酶-3/9,基质金属蛋白酶(MMP)-2/9,波形蛋白,AKT,PI3K和mTOR的蛋白表达水平。使用qRT-PCR检查hsa-circ-0072309和miR-100的表达。通过膜联蛋白v-FITC / PI用流式细胞仪和改良的两腔迁移分析或Millicell悬浮细胞培养分别确定凋亡率和迁移或侵袭率。结果:hsa-circ-0072309在肿瘤组织中表达较差。丰富的hsa-circ-0072309诱导了细胞增殖,迁移和侵袭的抑制,以及PI3K / AKT和mTOR级联的抑制,但凋亡的增强。 circRNA刺激了miR-100的下调,miR-100在肿瘤组织中低表达,并且其过量产生消除了circRNA对上述这些元件的影响。结论:hsa-circ-0072309通过在CAKI-1和ACHN细胞系中阻断PI3K / AKT和mTOR级联来靶向miR-100,从而发挥抗肿瘤作用。

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