Silencing miRNA-1297 suppresses the invasion and migration of prostate cancer cells via targeting modulation of PTEN and blocking of the AKT/ERK pathway.

Silencing miRNA-1297 suppresses the invasion and migration of prostate cancer cells via targeting modulation of PTEN and blocking of the AKT/ERK pathway.
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DOI:
10.3892/etm.2021.10200
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发表时间:
2021-07
影响因子:
2.7
通讯作者:
Kang S
Kang S
中科院分区:
医学4区
文献类型:
--
作者:
Wang L;Gao J;Zhang Y;Kang S

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磷酸酶和张力蛋白同源基因(PTEN)缺失是前列腺癌(PC)的主要致病因素。据报道,miRNA-1297在多种癌症类型中发挥作用;然而,miRNA-1297在PC中的潜在作用尚未被研究。在本研究中,肿瘤及邻近组织收集自PC患者。聚合酶链式反应检测miRNA-1297基因表达水平。结果表明,miRNA-1297在PC患者的肿瘤组织和PC细胞系中过表达。MiRNA-1297也促进了PC的进展。PTEN被确认为miRNA-1297的直接靶点,并通过四个结合位点与miRNA-1297结合。MiRNA-1297水平与PTEN水平呈负相关。沉默miRNA-1297或过表达PTEN可显著抑制细胞的迁移和侵袭。此外,当miRNA-1297沉默或PTEN过表达后,AKT/ERK通路也受到抑制。这些结果表明,沉默miRNA-1297可能通过调节PTEN和阻断AKT/ERK通路来抑制PC细胞的侵袭和迁移。本研究结果为前列腺癌的治疗提供了新的策略。
Phosphatase and tensin homolog (PTEN) loss is a major contributing factor of prostate cancer (PC). miRNA-1297 was reported to serve role in various cancer types; however, the potential roles of miRNA-1297 in PC had not been investigated. In the present study, tumor and adjacent tissues were collected from patients with PC. The gene expression level of miRNA-1297 was measured via polymerase chain reaction. Results indicated that the miRNA-1297 was overexpressed in tumor tissues from PC patients and in PC cell lines. miRNA-1297 also contributed toward the progression of PC. PTEN was confirmed as the direct target of miRNA-1297 and bound with miRNA-1297 via four binding sites. The miRNA-1297 level was negatively associated with the PTEN level. Silencing miRNA-1297 or overexpression of PTEN significantly inhibited the cell migration and invasion. In addition, the AKT/ERK pathway was also inhibited following silencing of miRNA-1297 or overexpression of PTEN. Taken together, the results indicated that silencing miRNA-1297 exerted inhibitory effects on the invasion and migration of PC cells via modulating PTEN and blocking of the AKT/ERK pathway. The results of the present study provided a novel strategy for treatment of prostate cancer cells.
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