FHIT Suppresses Epithelial-Mesenchymal Transition (EMT) and Metastasis in Lung Cancer through Modulation of MicroRNAs SCIE SCOPUS

Cited 45 time in WEB OF SCIENCE Cited 49 time in Scopus
Title
FHIT Suppresses Epithelial-Mesenchymal Transition (EMT) and Metastasis in Lung Cancer through Modulation of MicroRNAs
Author(s)
Suh, Sung-Suk; Yoo, Ji Young; Cui, Ri; Kaur, Balveen; Huebner, Kay; Lee, Taek-Kyun; Aqeilan, Rami I.; Croce, Carlo M.
KIOST Author(s)
Lee, Taek Kyun(이택견)
Publication Year
2014-10
Abstract
Metastasis is the principal cause of cancer death and occurs through multiple, complex processes that involve the concerted action of many genes. A number of studies have indicated that the Fragile Histidine Triad (FHIT) gene product, FHIT, functions as a tumor suppressor in a variety of common human cancers. Although there are suggestions of a role for FHIT loss in progression of various cancers, a role for such loss in metastasis has not been defined. Here, via in vivo and in vitro assays, we reveal that the enforced expression of FHIT significantly suppresses metastasis, accompanied by inhibition of the epithelial-mesenchymal transition (EMT), a process involved in metastasis through coordinate modulation of EMT-related genes. Specifically, miR-30c, a FHIT-upregulated microRNA, contributes to FHIT function in suppression of EMT and metastasis by directly targeting metastasis genes Metadherin (MTDH), High-mobility group AT-hook 2 (HMGA2), and the mesenchymal markers, Vimentin (VIM) and Fibronectin (FN1), in human lung cancer. Finally, we demonstrate that the expression pattern of FHIT and miR-30c is inversely correlated with that of MTDH and HMGA2 in normal tissue, non-metastatic and metastatic tumors, serving as a potential biomarker for metastasis in lung cancer.
ISSN
1553-7404
URI
https://sciwatch.kiost.ac.kr/handle/2020.kiost/2702
DOI
10.1371/journal.pgen.1004652
Bibliographic Citation
PLOS GENETICS, v.10, no.10, 2014
Publisher
PUBLIC LIBRARY SCIENCE
Subject
TGF-BETA; PROTEIN EXPRESSION; GENE; GROWTH; PROGNOSIS; APOPTOSIS; 3P14.2; CELLS; IDENTIFICATION
Type
Article
Language
English
Document Type
Article
Publisher
PUBLIC LIBRARY SCIENCE
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