Open AccessmiR‐522 facilitates the prosperities of endometrial carcinoma cells by directly binding to monoamine oxidase B
Author(s) -
Zhang HongChang,
Han YanYan,
Zhang XinMin,
Xiao Nan,
Jiang Tao,
Zhu Shuang,
Wang EnPeng,
Chen ChangBao
Publication year - 2019
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12107
Subject(s) - endometrial cancer , medicine , cancer research , carcinoma , monoamine oxidase , carcinogenesis , microrna , downregulation and upregulation , monoamine oxidase b , oncology , cancer , gene , enzyme , biology , genetics , biochemistry
It is well known that microRNAs (miRNAs) are crucial regulatory factors in tumorigenesis, as tumor suppressors or cancer‐promoting factors. However, the study of endometrial carcinoma relevance in miR‐522 is rare, indicating an undefined molecular mechanism for its role. Therefore, we performed this study to examine the role of miR‐522 on the biological behaviors of endometrial carcinoma. In this work, we found that miR‐522 was highly expressed in endometrial carcinoma and negatively regulated monoamine oxidase B (MAOB) expression. They also have the opposite effect on prognosis of endometrial carcinoma patients. More importantly, miR‐522 could decreased MAOB expression by binding to MAOB with a putative site, thereby promoting cell proliferation, migration, and invasion through in vitro functional analyses, including MTT assay, wound‐healing and transwell invasion experiments. Upregulation of MAOB rescued the impacts of miR‐522 mimic on cell behaviors. In conclusion, our observations demonstrated that miR‐522 accelerated the progression of endometrial carcinoma by inhibiting MAOB, which might lead to a novel therapeutic therapy for endometrial carcinoma.