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Repression of Micro RNA ‐372 by Arsenic Sulphide Inhibits Prostate Cancer Cell Proliferation and Migration through Regulation of large tumour suppressor kinase 2
Author(s) -
Cao Hongwen,
Feng Yigeng,
Chen Lei
Publication year - 2017
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.12687
Subject(s) - prostate cancer , cancer research , cell growth , oncogene , cancer , microrna , cell , suppressor , cell migration , kinase , chemistry , biology , cell cycle , microbiology and biotechnology , medicine , gene , biochemistry
As the main component of realgar, arsenic sulphide (As 4 S 4 ) contains antitumour activity by repressing cancer cell proliferation and migration in many tumours. However, the detailed mechanism of these processes is not clear yet. Micro RNA s (mi RNA s) can function as tumour suppressor or oncogene based on their target mRNA s in different tumour tissues. Here, we found that As 4 S 4 could repress the overexpression of micro RNA ‐372 (miR‐372) in two prostate cancer cell lines and its overexpression promoted cell proliferation and migration. Large tumour suppressor kinase 2 ( LATS 2) was confirmed as a direct target of miR‐372 using luciferase assays in these two prostate cancer cell lines. Down‐regulation of LATS 2 could promote prostate cancer cell proliferation and migration just as overexpression of miR‐372 did and overexpression of LATS 2 could reverse this effect of miR‐372. The antitumour activity of As 4 S 4 and the oncogenic function of miR‐372 were further confirmed using a mouse xenograft model. Altogether, our data showed evidence that repressing the overexpression of miR‐372 by As 4 S 4 could inhibit prostate cancer cell proliferation and migration by targeting LATS 2. Therefore, miR‐372 may be a possible biomarker for the prediction of prostate cancer and As 4 S 4 may have potential therapeutic function for prostate cancer.
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