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MTF2 通过激活蜗牛家族转录抑制因子来诱导肝细胞癌的上皮-间质转化和进展
Authors Wu TT, Cai J, Tian YH, Chen JF, Cheng ZL, Pu CS, Shi WZ, Suo XP, Wu XJ, Dou XW, Zhang KM
Received 6 August 2019
Accepted for publication 31 October 2019
Published 17 December 2019 Volume 2019:12 Pages 11207—11220
DOI https://doi.org/10.2147/OTT.S226119
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Sanjay Singh
Background: Metal regulatory transcription factor 2 (MTF2) has been previously reported as a protein binding to the metal response element of the mouse metallothionein promoter, which is involved in chromosome inactivation and pluripotency. However, the function of MTF2 in tumor formation and progression has not yet been completely elucidated.
Methods: The expression of MTF2 and clinicopathological characteristics were evaluated by hepatocellular carcinoma (HCC) tissue microarray of 240 specimens. The role of MTF2 on HCC progression was determined using MTT, crystal violet, and transwell assays. Tumor growth was monitored in a xenograft model, and intrahepatic metastasis models were established.
Results: The expression of MTF2 was increased in HCC and strongly associated with the clinical characteristics and prognosis. Forced expression of MTF2 in HCC cells significantly promoted cell growth, migration, and invasion in vitro. In contrast, downregulation of MTF2 inhibited cell growth, migration, and invasion in vitro. Moreover, knock down of MTF2 suppressed tumorigenesis and intrahepatic metastasis of HCC cells in vivo. Mechanistically, MTF2 overexpression may promote growth and epithelial-mesenchymal transition processes of HCC cells by facilitating Snail transcription.
Conclusion: MTF2 promotes the proliferation, migration, and invasion of HCC cells by regulating Snail transcription, providing a potential therapeutic candidate for patients with HCC.
Keywords: MTF2, progression, hepatocellular carcinoma, EMT, Snail