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微小RNA-372通过直接靶向大肿瘤抑制因子2促进乳腺癌细胞增殖。

miR-372 promotes breast cancer cell proliferation by directly targeting LATS2.

作者信息

Cheng Xueyuan, Chen Junqiang, Huang Zhong

机构信息

Department of Gastrointestinal Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.

Department of General Surgery, Beihai People's Hospital, Beihai, Guangxi 536000, P.R. China.

出版信息

Exp Ther Med. 2018 Mar;15(3):2812-2817. doi: 10.3892/etm.2018.5761. Epub 2018 Jan 17.

DOI:10.3892/etm.2018.5761
PMID:29456685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5795589/
Abstract

MicroRNAs (miRs) have previously been demonstrated to be important in the tumorigenesis and progression of breast cancer. miR-372 was previously revealed to be involved in various types of human cancer, however its function in breast cancer remains largely unknown. The present study demonstrated that miR-372 is frequently overexpressed in breast cancer cell lines and tissues. The downregulation of miR-372 markedly inhibited cell proliferation, arrested the cell cycle in the G1/S phase, and increased the apoptosis of breast cancer cells. Consistently, an xenograft study also demonstrated the suppressive effects of miR-372 knockdown on tumor growth. Further studies revealed that miR-372 modulated the expression of large tumor suppressor kinase 2 (LATS2) by directly targeting its 3'-untranslated region in breast cancer cells. Furthermore, silencing of LATS2 was able to rescue the effect of the miR-372 inhibitor. Overall, the results suggest that miR-372 functions as an oncogenic miRNA in breast cancer by targeting LATS2.

摘要

微小RNA(miR)先前已被证明在乳腺癌的发生和发展中起重要作用。miR-372先前已被揭示参与多种类型的人类癌症,然而其在乳腺癌中的功能仍 largely未知。本研究表明,miR-372在乳腺癌细胞系和组织中经常过度表达。miR-372的下调显著抑制细胞增殖,使细胞周期停滞在G1/S期,并增加乳腺癌细胞的凋亡。同样,一项异种移植研究也证明了miR-372敲低对肿瘤生长的抑制作用。进一步的研究表明,miR-372通过直接靶向乳腺癌细胞中大型肿瘤抑制激酶2(LATS2)的3'-非翻译区来调节其表达。此外,LATS2的沉默能够挽救miR-372抑制剂的作用。总体而言,结果表明miR-372通过靶向LATS2在乳腺癌中作为致癌性微小RNA发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/3e3760e58b40/etm-15-03-2812-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/086359795a18/etm-15-03-2812-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/47a3ad4db600/etm-15-03-2812-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/fdf3660d505a/etm-15-03-2812-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/017e4459c9ff/etm-15-03-2812-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/3e3760e58b40/etm-15-03-2812-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/086359795a18/etm-15-03-2812-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/47a3ad4db600/etm-15-03-2812-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/fdf3660d505a/etm-15-03-2812-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/017e4459c9ff/etm-15-03-2812-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d4e/5795589/3e3760e58b40/etm-15-03-2812-g05.jpg

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