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Arsenic targets Pin1 and cooperates with retinoic acid to inhibit cancer-driving pathways and tumor-initiating cells
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Arsenic targets Pin1 and cooperates with retinoic acid to inhibit cancer-driving pathways and tumor-initiating cells
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Journal Article
Arsenic targets Pin1 and cooperates with retinoic acid to inhibit cancer-driving pathways and tumor-initiating cells
2018
Overview
Arsenic trioxide (ATO) and all-
trans
retinoic acid (ATRA) combination safely cures fatal acute promyelocytic leukemia, but their mechanisms of action and efficacy are not fully understood. ATRA inhibits leukemia, breast, and liver cancer by targeting isomerase Pin1, a master regulator of oncogenic signaling networks. Here we show that ATO targets Pin1 and cooperates with ATRA to exert potent anticancer activity. ATO inhibits and degrades Pin1, and suppresses its oncogenic function by noncovalent binding to Pin1’s active site. ATRA increases cellular ATO uptake through upregulating aquaporin-9. ATO and ATRA, at clinically safe doses, cooperatively ablate Pin1 to block numerous cancer-driving pathways and inhibit the growth of triple-negative breast cancer cells and tumor-initiating cells in cell and animal models including patient-derived orthotopic xenografts, like Pin1 knockout, which is substantiated by comprehensive protein and microRNA analyses. Thus, synergistic targeting of Pin1 by ATO and ATRA offers an attractive approach to combating breast and other cancers.
Arsenic trioxide and all-
trans
retinoic acid combination safely cures human acute promyelocytic leukemia. Here, the authors show that this combination has potent anticancer activity in triple negative breast cancer by cooperatively targeting Pin1, a master regulator of oncogenic signaling networks, to eliminate cancer stem cells.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 96/1
/ 96/100
/ 96/106
/ 96/109
/ 96/31
/ 96/44
/ 96/63
/ 96/95
/ Animals
/ Antineoplastic Agents - pharmacology
/ Arsenic
/ Arsenic Trioxide - pharmacology
/ Cancer
/ Cures
/ Female
/ Gene Expression Regulation, Neoplastic
/ Humanities and Social Sciences
/ Humans
/ Leukemia
/ Leukemia, Promyelocytic, Acute - metabolism
/ Liver
/ Magnetic Resonance Spectroscopy
/ Mice
/ miRNA
/ NIMA-Interacting Peptidylprolyl Isomerase - metabolism
/ Proteins
/ RNA
/ Science
/ Tumors
