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沉默miRNA-1297通过靶向调控PTEN和阻断AKT/ERK信号通路抑制前列腺癌细胞的侵袭和迁移。

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

作者信息

Wang Lei, Gao Jing, Zhang Yu, Kang Shaosan

机构信息

Department of Urology, North China University of Science and Technology Affiliated Hospital, Tangshan, Hebei 063000, P.R. China.

Department of Obstetrics and Gynecology, Tangshan Hongci Hospital, Tangshan, Hebei 063000, P.R. China.

出版信息

Exp Ther Med. 2021 Jul;22(1):768. doi: 10.3892/etm.2021.10200. Epub 2021 May 17.

DOI:10.3892/etm.2021.10200
PMID:34055067
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8145438/
Abstract

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.

摘要

磷酸酶和张力蛋白同源物（PTEN）缺失是前列腺癌（PC）的一个主要促成因素。据报道，miRNA - 1297在多种癌症类型中发挥作用；然而，miRNA - 1297在PC中的潜在作用尚未得到研究。在本研究中，收集了PC患者的肿瘤组织和相邻组织。通过聚合酶链反应测量miRNA - 1297的基因表达水平。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的直接靶标，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显著抑制细胞迁移和侵袭。此外，沉默miRNA - 1297或过表达PTEN后，AKT/ERK途径也受到抑制。综上所述，结果表明沉默miRNA - 1297通过调节PTEN和阻断AKT/ERK途径对PC细胞的侵袭和迁移发挥抑制作用。本研究结果为前列腺癌细胞的治疗提供了一种新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/0eba91a6a744/etm-22-01-10200-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/1dc69c72d86c/etm-22-01-10200-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/5d79bef948c8/etm-22-01-10200-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/3236eac28c4e/etm-22-01-10200-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/23b7bfb7df99/etm-22-01-10200-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/0eba91a6a744/etm-22-01-10200-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/1dc69c72d86c/etm-22-01-10200-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/5d79bef948c8/etm-22-01-10200-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/3236eac28c4e/etm-22-01-10200-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/23b7bfb7df99/etm-22-01-10200-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f648/8145438/0eba91a6a744/etm-22-01-10200-g04.jpg

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