The Prognostic Significance of the TEAD4 in Hepatocellular Carcinoma

• Published in: International journal of general medicine Vol. 16; pp. 6005 - 6013
• Main Authors: Lei, Liping, Yang, Jingjing, Peng, Hao, Huang, Ruiyan, Liang, Lichun, Liu, Ruifang, Li, Jiangfa
• Format: Journal Article
• Language: English
• Published: New Zealand Dove Medical Press Limited 31-12-2023; Dove; Dove Medical Press
• Subjects: Analysis; Cancer; Cancer patients; Development and progression; Genetic aspects; Genomics; hepatocellular carcinoma; Hepatoma; Liver; Metastasis; Original Research; Prognosis; tcga; tead4; Type 2 diabetes; TEAD4; TCGA; hepatocellular carcinoma
• ISSN: 1178-7074; 1178-7074
• DOI: 10.2147/IJGM.S440973

Abnormal expression of genes causes tumorigenesis, tumor progression, and poor prognosis in hepatocellular carcinoma (HCC). Therefore, the aims of this study were to explore the transcription enhancer domain factor 4 (TEAD4) in patients with liver cancer and its relationship with prognosis.
HTSeq-FPKM data and corresponding clinical data of HCC patients were obtained from The Cancer Genome Atlas (TCGA). Difference in TEAD4 expression between normal and tumor and the correlation with clinical characteristics were analyzed by the chi-squared test based on UALCAN. HepG2 cell lines were used to study the effect of TEAD4 on HCC cell lines. The expression and clinical significance of TEAD4 in HCC were detected in clinical cases.
The transcription and post-transcription levels of TEAD4 were higher in HCC tumors than normal illustrated different expressed transcription of TEAD4 in gender, nodal metastasis status, tumor grades, and individual cancer stages. The high TEAD4 expression was significantly associated with tumor grades. The high expression of TEAD4 was significantly correlated to shorter 2-5 years overall survival. Inhibition of TEAD4 expression in HepG2 cells resulted in significantly decreased cell proliferation and invasion.
TEAD4 was identified as an independent prognostic factor, and inhibition of TEAD4 expression in HepG2 cells resulted in significantly decreased cell proliferation and invasion.