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 ABH...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.展开更多
基金supported by the Quanzhou High-Level Talents Project(2021C048R).
文摘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.
