Jun 6, 2020 · During heart development, the PRMT1-p53 pathway is required for epicardial invasion and formation of epicardial-derived lineages: cardiac fibroblasts, coronary smooth muscle cells, and pericytes. Consequently, this pathway modulates ventricular morphogenesis and coronary vessel formation.

This study elucidates a role for p53 in regulating EMT-MET (mesenchymal-epithelial transition) and stemness or differentiation plasticity, and reveals a potential therapeutic implication to suppress EMT-associated cancer stem cells through activation of the p53-miR-200c pathway.

As p53 is a crucial tumor suppressor and EMT/stemness is implicated as an important aspect in tumor initiation and malignant progression, the authors further analyzed the impact of miR-200c activation by p53 in cancer cells.

Jun 9, 2020 · During heart development, the PRMT1-p53 pathway is required for epicardial invasion and formation of epicardial-derived lineages: cardiac fibroblasts, coronary smooth muscle cells, and pericytes. Consequently, this pathway modulates ventricular morphogenesis and coronary vessel formation.

Interestingly, p53 has been shown to mediate its effects via the miRNA-dependent mechanism that targets master-regulators of EMT, such as Zeb1/2, Snail, Slug, and Twist1. This regulation often involves interactions of miRNAs with lncRNAs.

Jan 4, 2021 · In this review, we present a detailed overview of miRNA/lncRNA-dependent mechanisms that control interplay between p53 and master-regulators of EMT and their importance for breast cancer.

PRMT1 regulates splicing of Mdm4 and decreases p53 stability, which enhances Slug degradation to block epicardial EMT. The PRMT1-p53 axis is required for epicardial invasion and formation of epicardial-derived lineages during development.

May 5, 2019 · Epithelial-mesenchymal transition (EMT) involves metastasis and drug resistance; thus, a new EMT reversing agent is required. It has shown that wild-type p53 can reverse EMT back to epithelial characteristics, and iron chelator acting as …

May 1, 2024 · Loss of p53/Gain of function mutation in p53 activates the EMT programme, accompanied by an increased stem cell population via modulating the expression profile of various EMT-TFs including ZEB1, SNAI1.

Jul 30, 2012 · Here, we report that mutant p53 exerts oncogenic functions and promotes EMT in endometrial cancer (EC) by directly binding to the promoter of miR-130b (a negative regulator of ZEB1) and...