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首页> 外文期刊>Journal of cellular biochemistry. >microRNA‐383 suppresses the PI3K‐AKT‐MTOR signaling pathway to inhibit development of cervical cancer via down‐regulating PARP2
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microRNA‐383 suppresses the PI3K‐AKT‐MTOR signaling pathway to inhibit development of cervical cancer via down‐regulating PARP2

机译：microRNA-383抑制PI3K-AKT-MTOR信号通路，通过下调PARP2抑制宫颈癌的发育

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Abstract This study aims to evaluate the effect of the regulatory relationship between microRNA‐383 (miR‐383) and PARP2 in the cell migration and invasion in human with cervical cancer (CC) via the PI3K‐AKT‐MTOR signaling pathway. Cancerous tissues and corresponding paracancerous tissues were collected from 115 patients with CC. The positive expression rate of PARP2 was detected by immunohistochemistry. HeLa cells with highest miR‐383 expression were selected and assigned into the blank, negative control (NC), miR‐383 mimic, miR‐383 inhibitor, si‐PARP2, and miR‐383 inhibitor?+?si‐PARP2 groups. qRT‐PCR and Western blot were performed to evaluate the expression of miR‐383, PI3K, AKT, mTOR, PARP2, and p70S6K. MTT assay were utilized to measure cell viability. Transwell assay were applied to evaluate cell invasion and metastasis. Dual luciferase reporter assay identified that PARP2 is a target gene of miR‐383. Cancerous tissues manifested higher expression of PI3K, AKT, mTOR, PARP2, and p70S6K but lower miR‐383 expression than paracancerous tissues. Compared with the blank and NC groups, the miR‐383 mimic and si‐PARP2 groups had decreased expression of PI3K, AKT, mTOR, PARP2, and p70S6K mRNA and protein. In the miR‐383 mimic and si‐PARP2 groups, the cell viability, migration, and invasion were descended, in comparison to the blank and NC groups. All above parameters showed an opposite trend in the miR‐383 inhibitor group when compared with the blank and NC groups. This study demonstrates that miR‐383 could down‐regulate PARP2 to protect against CC by inhibiting PI3K‐AKT‐MTOR signaling pathway.
机译：摘要本研究旨在通过PI3K-AKT-MTOR信号通路评估MicroRNA-383（miR-383）和PARP2在人体血癌（CC）中的细胞迁移和侵袭之间的调节关系的影响。从115例CC患者收集癌组织和相应的副癌组织。免疫组织化学检测PARP2的阳性表达率。选择具有最高miR-383表达的HeLa细胞，并分配到坯料，阴性对照（NC），miR-383模拟物，miR-383抑制剂，Si-PARP2和MIR-383抑制剂？+？Si-PARP2组中。进行QRT-PCR和Western印迹以评估miR-383，Pi3k，Akt，MTOR，PARP2和P70S6K的表达。 MTT测定用于测量细胞活力。施用Transwell测定来评估细胞侵袭和转移。双荧光素酶报告结果确定PARP2是miR-383的靶基因。癌组织表现出pi3k，akt，mtor，parp2和p70s6k的更高表达，但比副癌组织更低的miR-383表达。与坯料和NC组相比，MIR-383模拟和Si-PARP2组的表达降低了PI3K，AKT，MTOR，PARP2和P70S6K mRNA和蛋白质的表达。在MiR-383模拟和Si-PARP2组中，与坯料和NC组相比，降低细胞活力，迁移和侵袭。与坯料和NC组相比，上述所有参数显示MIR-383抑制剂组的相反趋势。该研究表明MIR-383可以通过抑制PI3K-AKT-MTOR信号通路来降低PARP2以防止CC。

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