miR-491-5p functions as a tumor suppressor by targeting JMJD2B in ERα-positive breast cancer.
The involvement of miR-491-5p in breast cancer development is unclear. This study showed that miR-491-5p is significantly downregulated in ERα-positive breast cancer tissues and cell lines and is generally hypermethylated in ERα-positive breast cancer. MiR-491-5p overexpression significantly suppressed estrogen signaling and estrogen-stimulated proliferation of breast cancer cells. Furthermore, the histone demethylase JMJD2B was identified as a direct target of miR-491-5p. The ectopic expression of JMJD2B abrogated the phenotypic changes induced by miR-491-5p in breast cancer cells. Collectively, our data indicate that miR-491-5p plays a tumor suppressor role in the development and progression of breast caner and may be a novel therapeutic target against ERα-positive breast cancer.
The 3rd Division of Oncology of the People's Hospital of Huangpi District and the Third Affiliated Hospital of Jianghan University, Wuhan 430300, China.
Zeng
Z
Hui
Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan 430074, China.
Chen
C
Yiling
Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan 430074, China.
You
Y
Wenting
Department of Medical Oncology, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, 435000, China.
Huang
H
XuQun
Department of Radiation Oncology Yueyang Second People's Hospital, Yueyang 414000, China.
Zhou
Z
ChuanYi
Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan 430074, China. Electronic address: huili0930@mail.hust.edu.cn.
Li
L
Hui
D020413:3' Untranslated Regions; D000328:Adult; D000368:Aged; D001374:Azacitidine / Q000031:analogs & derivatives / Q000494:pharmacology; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D019175:DNA Methylation; D000077209:Decitabine; D047628:Estrogen Receptor alpha / Q000378:metabolism*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D006801:Humans; D056484:Jumonji Domain-Containing Histone Demethylases / Q000235:genetics* / Q000378:metabolism; D061986:MCF-7 Cells; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism*; D008875:Middle Aged
D020413:3' Untranslated Regions; D047628:Estrogen Receptor alpha; C551410:MIRN491 microRNA, human; D035683:MicroRNAs; D000077209:Decitabine; D056484:Jumonji Domain-Containing Histone Demethylases; C523637:KDM4B protein, human; D001374:Azacitidine
Breast cancer; Estrogen receptor α; Estrogen signaling; JMJD2B; miR-491-5p