2. Academic Validation
  3. Suppressing MTERF3 inhibits proliferation of human hepatocellular carcinoma via ROS-mediated p38 MAPK activation

Suppressing MTERF3 inhibits proliferation of human hepatocellular carcinoma via ROS-mediated p38 MAPK activation

  • Commun Biol. 2024 Jan 5;7(1):18. doi: 10.1038/s42003-023-05664-7.
Zhihai Zheng # 1,  Youjuan Zhao # 2,  Hongjia Yu # 2,  Tingting Wang 3,  Jinhai Li 4,  Liang Xu 2,  Chunming Ding 2,  Lan He 5,  Lijun Wu 6,  Zhixiong Dong 7
Affiliations

Affiliations

  • 1 Department of Colorectal Surgery, The First Affiliated Hospital of Wenzhou Medical University, 2 Fuxue Lane, Wenzhou, Zhejiang, 325000, China.
  • 2 Zhejiang Provincial Key Laboratory of Medical Genetics, Key Laboratory of Laboratory Medicine, Ministry of Education, China, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
  • 3 Department of Gastroenterology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
  • 4 Department of Liver and Gall Surgery, The Third Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325200, Zhejiang, China.
  • 5 School of Biomedical Science, Hunan University, Changsha, Hunan, 410013, PR China. helan2019@hnu.edu.cn.
  • 6 Department of Hepatobiliary Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. wumolijun@163.com.
  • 7 Zhejiang Provincial Key Laboratory of Medical Genetics, Key Laboratory of Laboratory Medicine, Ministry of Education, China, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. dongzx882@163.com.
  • # Contributed equally.
PMID: 38177713 DOI: 10.1038/s42003-023-05664-7
Abstract

Mitochondrial transcription termination factor 3 (MTERF3) negatively regulates mitochondrial DNA transcription. However, its role in hepatocellular carcinoma (HCC) progression remains elusive. Here, we investigate the expression and function of MTERF3 in HCC. MTERF3 is overexpressed in HCC tumor tissues and higher expression of MTERF3 positively correlates with poor overall survival of HCC patients. Knockdown of MTERF3 induces mitochondrial dysfunction, S-G2/M cell cycle arrest and Apoptosis, resulting in cell proliferation inhibition. In contrast, overexpression of MTERF3 promotes cell cycle progression and cell proliferation. Mechanistically, mitochondrial dysfunction induced by MTERF3 knockdown promotes ROS accumulation, activating p38 MAPK signaling pathway to suppress HCC cell proliferation. In conclusion, ROS accumulation induced by MTERF3 knockdown inhibits HCC cell proliferation via p38 MAPK signaling pathway suggesting a promising target in HCC patients.

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