Open AccessT Cell Factor 4 Is Involved in Papillary Thyroid Carcinoma via Regulating Long Non-Coding RNA HCP5
Author(s) -
Rui Wang,
Jinzhen Cai,
Shaolin Xie,
Cheng Zhao,
Yi Wang,
Deming Cao,
Gang Li
Publication year - 2020
Publication title -
technology in cancer research and treatment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.754
H-Index - 63
eISSN - 1533-0346
pISSN - 1533-0338
DOI - 10.1177/1533033820983290
Subject(s) - gene knockdown , wnt signaling pathway , tcf4 , cancer research , biology , thyroid carcinoma , cell growth , microbiology and biotechnology , transcription factor , chemistry , cell culture , signal transduction , gene , thyroid , endocrinology , genetics , enhancer
The annual incidence of papillary thyroid carcinoma has increased dramatically. T cell factor 4 (TCF4) is an important component of Wnt signaling pathway.However, the role of TCF4 in PTC remains unknown. In this study, TCF4 was observed to overexpress in PTC patients and cells by qRT-PCR assay. The colony formation assay, Edu staining and transwell assay indicated thatoverexpression of TCF4 promoted cell proliferation and invasion of TCP-1 cells, whereas knockdown of TCF4 inhibited cell proliferation and invasion of IHH-4 cells. To investigate the mechanism of TCF4 in PTC cells, the luciferase assay demonstrated that TCF4 could modulate HCP5 expression. Besides, GLuc-ON promoter reporter assayproved that TCF4 could bind to HCP5 promoter. Further, knockdown of HCP5 could significantly up-regulated miR-15a, miR-216a-5p, miR-22-3p, miR-139-5p, miR-203, miR-27a-3p and miR-320, and down-regulated miR-186-5p in IHH-4 cells, which might be potential downstream of TFC4/HCP5 axis. In conclusion, up-regulation TCF4 can promote HCP5 expression via binding to HCP5 promoter. It may be the first time to prove that TCF4 regulates HCP5 in PTC, which provides a novel sight for treatment of PTC.