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MTA 1‐activated Epi‐micro RNA ‐22 regulates E‐cadherin and prostate cancer invasiveness
Author(s) -
Dhar Swati,
Kumar Avinash,
Gomez Christian R.,
Akhtar Israh,
Hancock John C.,
Lage Janice M.,
Pound Charles R.,
Levenson Anait S.
Publication year - 2017
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12603
Subject(s) - prostate cancer , microrna , cadherin , cancer research , metastasis , ectopic expression , epigenetics , epithelial–mesenchymal transition , biology , cancer , cell , cell culture , gene , genetics
We have previously shown that metastasis‐associated protein 1 ( MTA 1), a chromatin remodeler, plays an important role in prostate cancer invasiveness, likely through regulation of epithelial‐to‐mesenchymal transition. Here, we identified miR‐22 as an epigenetic‐micro RNA (Epi‐miR) directly induced by MTA 1 and predicted to target E‐cadherin. Loss‐of‐function and overexpression studies of MTA 1 reinforced its regulatory role in miR‐22 expression. MiR‐22 directly targets the 3′‐untranslated region of E‐cadherin, and ectopic overexpression of miR‐22 diminishes E‐cadherin expression. Overexpression of miR‐22 in prostate cancer cells promotes cell invasiveness and migration. Meta‐analysis of patient tumor samples indicates a positive correlation between MTA 1 and miR‐22, supporting their inhibitory effect on E‐cadherin expression. Our findings implicate the MTA 1/Epi‐miR‐22/E‐cadherin axis as a new epigenetic signaling pathway that promotes tumor invasion in prostate cancer.