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Research Paper|Volume 14, Issue 4|pp 1743—1766

THRSP identified as a potential hepatocellular carcinoma marker by integrated bioinformatics analysis and experimental validation

Yuxi Ding1,2,3, Xiaoling Liu1,2,3, Yue Yuan1,2,3, Yunjian Sheng1,2,3, Decheng Li1,2,3, Suvash Chandra Ojha1,2,3, Changfeng Sun1,2,3, Cunliang Deng1,2,3
  • 1The Department of Infectious Diseases, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China
  • 2The Department of Tuberculosis, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China
  • 3Laboratory of Infection and Immunity, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China
* Co-first author
Received: January 30, 2021Accepted: January 17, 2022Published: February 23, 2022
https://doi.org/10.18632/aging.203900

Copyright: © 2022 Ding et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Hepatocellular carcinoma (HCC) is the most common malignant liver tumor with high mortality and poor prognosis worldwide. This study aimed to identify hub genes and investigate the underlying molecular mechanisms in HCC progression by integrated bioinformatics analysis and experimental validation. Based on the Gene Expression Omnibus (GEO) databases and The Cancer Genome Atlas (TCGA), 12 critical differential co-expression genes were identified between tumor and normal tissues. Via survival analysis, we found higher expression of LCAT, ACSM3, IGF1, SRD5A2, THRSP and ACADS was associated with better prognoses in HCC patients. Among which, THRSP was selected for the next investigations. We found that THRSP mRNA expression was negatively correlated with its methylation and closely associated with clinical characteristics in HCC patients. Moreover, THRSP expression had a negative correlation with the infiltration levels of several immune cells (e.g., B cells and CD4+ T cells). qRT-PCR verified that THRSP was lower expressed in HCC tissues and cell lines compared with control. Silencing of THRSP promoted the migration, invasion, proliferation, and inhibited cell apoptosis of HCCLM and Huh7 cell lines. Decreased expression of THRSP promoted HCC progression by NF-κB, ERK1/2, and p38 MAPK signaling pathways. In conclusion, THRSP might serve as a novel biomarker and therapeutic target of HCC.