Open Access

ARTICLE

ABHD17C represses apoptosis and pyroptosis in hepatocellular carcinoma cells

by LINPEI WANG^1,2, JIAWEI WANG², CHUNFENG SHI², WEI WANG^2,*, JIAN WU^1,*

1 Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310030, China
2 Department of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, China

* Corresponding Authors: WEI WANG. Email: ; JIAN WU. Email:

(This article belongs to the Special Issue: Navigating the Interplay of Cancer, Autophagy, ER Stress, Cell Cycle and Apoptosis: Mechanisms, Therapies, and Future Directions)

BIOCELL 2024, 48(9), 1299-1310. https://doi.org/10.32604/biocell.2024.051756

Received 14 March 2024; Accepted 22 May 2024; Issue published 04 September 2024

Abstract

Background: Alpha/beta hydrolase domain-containing protein 17C (ABHD17C) is a depalmitoylation enzyme that removes the S-palmitoylation of targeted proteins. The hepatocellular carcinoma (HCC) cells SNU449 and Hep3B use ABHD17C as an oncogene; however, the exact mechanism of this action is yet unknown. Methods: The expression of ABHD17C in liver cancer tissues was analyzed by bioinformatics, and the expression of ABHD17C in clinical liver cancer tissues and adjacent normal tissues was detected. Then, the proliferative viability of HCC cells after overexpression or knockdown of ABHD17C was examined, and pyroptosis and apoptosis proteins were detected. Results: ABHD17C was overexpressed in human HCC tissues as well as numerous HCC cell lines. Depletion of ABHD17C caused reduced viability, cell cycle arrest, and defective invasion and migration in HCC cells, while overexpression of ABHD17C exhibited the opposite effect. Moreover, we discovered that the knockdown of ABHD17C resulted in enhanced apoptotic and pyroptotic phenotypes of HCC cells, whereas overexpression of ABHD17C attenuated such phenotypes. Conclusions: It suggests that ABHD17C contributes to HCC carcinogenesis, making it a promising target for medication treatment.

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