title: miR-154 inhibits EMT by targeting HMGA2 in prostate cancer cells.
abstract: Epithelial-mesenchymal transition (EMT) is a crucial process that plays an important role in the invasion and metastasis of human cancers. High-mobility group AT-hook 2 (HMGA2) has been found to be involved in the EMT program, with its aberrant expression having been observed in a variety of malignant tumors. However, the mechanisms regulating HMGA2 expression remain incompletely understood. The objective of this study was to investigate whether mir-154 plays a critical role in EMT by regulating HMGA2. The expression levels of HMGA2 were examined in four samples of prostate cancer (PCa) tissue and adjacent non-tumorous tissue by Western blot analysis. The effects of forced expression of miR-154 or HMGA2 knockdown on PCa cells were evaluated by cell migration and invasion assays and Western blot analysis. HMGA2 was upregulated in the PCa tissue samples compared with the adjacent normal ones. Forced expression of miR-154 or HMGA2 knockdown significantly reduced the migratory and invasive capabilities of PCa cells in vitro and inhibited EMT gene expression, increased the levels of E-cadherin, an epithelial marker, and decreased the levels of vimentin, a mesenchymal marker. HMGA2 is a direct target gene of miR-154 by dual-luciferase reporter assay. Our findings suggest that miR-154 plays a role in regulating EMT by targeting HMGA2. Understanding the targets and regulating pathways of miR-154 may provide new insights into the underlying pathogenesis of PCa.
authors.affiliation: State Key Laboratory of Reproductive Medicine, Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
authors.forename: Chen
authors.initials: C
authors.lastname: Zhu
authors.forename: Jie
authors.initials: J
authors.lastname: Li
authors.forename: Gong
authors.initials: G
authors.lastname: Cheng
authors.forename: Hai
authors.initials: H
authors.lastname: Zhou
authors.forename: Liangjun
authors.initials: L
authors.lastname: Tao
authors.forename: Hongzhou
authors.initials: H
authors.lastname: Cai
authors.forename: Pu
authors.initials: P
authors.lastname: Li
authors.forename: Qiang
authors.initials: Q
authors.lastname: Cao
authors.forename: Xiaobing
authors.initials: X
authors.lastname: Ju
authors.forename: Xiaoxin
authors.initials: X
authors.lastname: Meng
authors.forename: Meilin
authors.initials: M
authors.lastname: Wang
authors.forename: Zhengdong
authors.initials: Z
authors.lastname: Zhang
authors.forename: Chao
authors.initials: C
authors.lastname: Qin
authors.forename: Lixin
authors.initials: L
authors.lastname: Hua
authors.forename: Changjun
authors.initials: C
authors.lastname: Yin
authors.forename: Pengfei
authors.initials: P
authors.lastname: Shao
mesh_terms: D020413:3' Untranslated Regions; D001483:Base Sequence; D001665:Binding Sites; D045744:Cell Line, Tumor; D002465:Cell Movement; D058750:Epithelial-Mesenchymal Transition; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D025743:HMGA2 Protein / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference
chemical_list: D020413:3' Untranslated Regions; D025743:HMGA2 Protein; C561122:MIRN154 microRNA, human; D035683:MicroRNAs