The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma.
OBJECTIVE
Increased expression of miR-200c was recently reported in endometrial carcinoma compared with normal tissues. In this study, we evaluated the role of miR-200c in cell growth and drug sensitivity in endometrial carcinoma and investigated the underlying mechanisms.


METHODS
The expression of miR-200c in human endometrial tissues was detected by quantitative RT-PCR. The transfection with anti-miRNA (anti-miR) or the premature form of miRNA (pre-miR) was performed to regulate the level of expression of miRNA-200c in endometrial carcinoma cells, HEC-1A and Ishikawa. To identify the target genes for miR-200c, we performed mRNA microarray after pre-miR-200c transfection in HEC-1A cells.


RESULTS
We found that miR-200c expression was increased in endometrial carcinoma compared with normal endometrial tissues. Anti-miR or pre-miR-200c could regulate cell survival, proliferation, and apoptosis and affect cytotoxicity in endometrial cancer cells. Through mRNA microarray analysis, we found that miR-200c inhibits the expression of BRD7, which was recently reported as a potential tumor suppressor gene. MiR-200c regulated the translocation of β-catenin from the cytoplasm to the nucleus via inhibition of BRD7, resulting in increased expression of its transcriptional target genes, cyclinD1 and c-myc.


CONCLUSIONS
The interaction between miR-200c and BRD7 might have important roles in controlling growth of endometrial of cancer cells and suggest a novel target pathway for treatment of this cancer.
Department of Obstetrics and Gynecology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Young-Ae
YA
Park
Jeong-Won
JW
Lee
Jung-Joo
JJ
Choi
Hye-Kyung
HK
Jeon
YoungJae
Y
Cho
ChelHun
C
Choi
Tae-Joong
TJ
Kim
Nak Woo
NW
Lee
Byoung-Gie
BG
Kim
Duk-Soo
DS
Bae
D017209:Apoptosis / Q000502:physiology; D048708:Cell Growth Processes / Q000502:physiology; D045744:Cell Line, Tumor; D002868:Chromosomal Proteins, Non-Histone / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism*; D003593:Cytoplasm / Q000378:metabolism; D016889:Endometrial Neoplasms / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D019940:Genes, bcl-1; D016259:Genes, myc; D006801:Humans; D035683:MicroRNAs / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism*; D014162:Transfection; D015854:Up-Regulation; D051176:beta Catenin / Q000378:metabolism; D000092468:Bromodomain Containing Proteins
D002868:Chromosomal Proteins, Non-Histone; D035683:MicroRNAs; D051176:beta Catenin; C485694:BRD7 protein, human; D000092468:Bromodomain Containing Proteins; C495270:CTNNB1 protein, human; C533896:MIRN200 microRNA, human