Research has previously shown that metastasis-associated protein 1 (MTA1), a chromatin remodeler, plays an important role in prostate cancer invasiveness, likely through regulation of epithelial-to-mesenchymal transition. In their latest study, researchers from the University of Mississippi Medical Center identified miR-22 as an epigenetic-microRNA (Epi-miR) directly induced by MTA1 and predicted to target E-cadherin.

Loss-of-function and overexpression studies of MTA1 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 promoted cell invasiveness and migration. Meta-analysis of patient tumor samples indicated a positive correlation between MTA1 and miR-22, supporting their inhibitory effect on E-cadherin expression.

These findings implicate the MTA1/Epi-miR-22/E-cadherin axis as a new epigenetic signaling pathway that promotes tumor invasion in prostate cancer.


S. Dhar, A. Kumar, C. R. Gomez, I. Akhtar, J. C. Hancock, J. M. Lage, C. R. Pound, A. S. Levenson (2017) MTA1-activated Epi-microRNA-22 regulates E-cadherin and prostate cancer invasiveness FEBS Letters doi: 10.1002/1873-3468.12603 [abstract]

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