Publication Date:
2017-03-19
Description:
PTPRJ is known for its antiproliferative role. Loss of heterozygosity (LOH) of PTPRJ has frequently been observed in various human cancers including colorectal cancer (CRC), lung cancer and breast cancer. However, the function and mechanism of PTPRJ in CRC is not well understood. At the present study, we show that ectopic expression of PTPRJ inhibits cell growth, migration and invasiveness in CRC cell line HCT116. Moreover, PTPRJ inhibits the tumorigenecity of HCT116 in a xenograft tumor model. MiR-155, the well-known oncomiR in CRC, is identified as an upstream factor of PTPRJ. MiR-155 directly binds to the 3' untranslated region of PTPRJ mRNA and suppresses the mRNA and protein levels of PTPRJ. Furthermore, the growth-promoting and AKT signaling activation effect of miR-155 was abrogated by PTPRJ overexpression, and vice versa. Our study reveals the crucial role of miR-155/PTPRJ/AKT axis in proliferation and migration of CRC cells and suggests a therapeutic potential of PTPRJ.This article is protected by copyright. All rights reserved
Electronic ISSN:
0091-7419
Topics:
Biology
,
Chemistry and Pharmacology
,
Medicine
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