Hsa-mir-182 suppresses lung tumorigenesis through down regulation of RGS17 expression in vitro.
Lung cancer is one of the most devastating diseases worldwide. RGS17 is previously shown to be over-expressed in human lung adenocarcinomas and plays an important role in lung tumor growth. Here we have identified a miRNA, has-mir-182, involved in the regulation of RGS17 expression through two conserved sites located in its 3' UTR region. Consistently, endogenous RGS17 expression level is regulated by hsa-mir-182 in human lung cancer cell lines. Similar to the knockdown of RGS17, ectopic expression of hsa-mir-182 significantly inhibits lung cancer cell proliferation and anchorage-independent cell growth, which can be rescued by re-expression of RGS17. Taken together, these data have provided the first evidence of miRNA regulation of RGS17 expression in lung cancer.
Sun
Yihua
Y
Department of Thoracic Surgery, Fudan University, Shanghai Cancer Center, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Fang
Rong
R
Li
Chenguang
C
Li
Li
L
Li
Fei
F
Ye
Xiaolei
X
Chen
Haiquan
H
D020413:3' Untranslated Regions; D001665:Binding Sites; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D015536:Down-Regulation; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics*; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D020710:RGS Proteins / Q000235:genetics*
D020413:3' Untranslated Regions; D035683:MicroRNAs; C538984:Mirn182 microRNA, human; D020710:RGS Proteins; C550555:RGS17 protein, human