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c-Met、CREB1和EGFR通过AKT/GSK-3β/Snail信号通路参与miR-493-5p对前列腺癌上皮-间质转化的抑制作用。

c-Met, CREB1 and EGFR are involved in miR-493-5p inhibition of EMT via AKT/GSK-3β/Snail signaling in prostate cancer.

作者信息

Wang Song, Wang Xiao, Li Jiangfeng, Meng Shuai, Liang Zhen, Xu Xin, Zhu Yi, Li Shiqi, Wu Jian, Xu Mingjie, Ji Alin, Lin Yiwei, Liu Ben, Zheng Xiangyi, Xie Bo, Xie Liping

机构信息

Department of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, People's Republic of China.

Department of Urology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang Province, People's Republic of China.

出版信息

Oncotarget. 2017 Jul 19;8(47):82303-82313. doi: 10.18632/oncotarget.19398. eCollection 2017 Oct 10.

DOI:10.18632/oncotarget.19398
PMID:29137265
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5669891/
Abstract

miR-493-5p downregulation has emerged as a critical player in cancer progression yet, the underlying mechanisms of miR-493-5p expression pattern and its function in prostate cancer remains to be elucidated. Here, we illustrate that miR-493-5p is frequently downregulated in prostate cancer, at least partially due to altered DNA methylation. miR-493-5p functions as a tumor suppressor in prostate cancer cells. c-Met, CREB1 and EGFR are downstream target genes of miR-493-5p. miR-493-5p inhibits EMT via AKT/GSK-3β/Snail signaling in prostate cancer. Taken together, our study identified c-Met, CREB1, EGFR and miR-493-5p establish a regulatory loop in prostate cancer, which could prove useful in the development of effective and therapies against prostate cancer.

摘要

miR-493-5p的下调已成为癌症进展中的关键因素,然而,miR-493-5p在前列腺癌中的表达模式及其功能的潜在机制仍有待阐明。在此,我们证明miR-493-5p在前列腺癌中经常下调,至少部分原因是DNA甲基化改变。miR-493-5p在前列腺癌细胞中起肿瘤抑制作用。c-Met、CREB1和EGFR是miR-493-5p的下游靶基因。miR-493-5p通过AKT/GSK-3β/Snail信号通路抑制前列腺癌中的上皮-间质转化(EMT)。综上所述,我们的研究确定c-Met、CREB1、EGFR和miR-493-5p在前列腺癌中建立了一个调节环路,这可能有助于开发针对前列腺癌的有效治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/6eb91b20ce3c/oncotarget-08-82303-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/df5df4f74026/oncotarget-08-82303-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/a099a8f78272/oncotarget-08-82303-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/f76eacdb36f9/oncotarget-08-82303-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/1f596533d828/oncotarget-08-82303-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/59f39e66426f/oncotarget-08-82303-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/031e1184e4dd/oncotarget-08-82303-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/6eb91b20ce3c/oncotarget-08-82303-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/df5df4f74026/oncotarget-08-82303-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/a099a8f78272/oncotarget-08-82303-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/f76eacdb36f9/oncotarget-08-82303-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/1f596533d828/oncotarget-08-82303-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/59f39e66426f/oncotarget-08-82303-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/031e1184e4dd/oncotarget-08-82303-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db1/5669891/6eb91b20ce3c/oncotarget-08-82303-g007.jpg

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