ABHD17C, an enzyme in the depalmitoylation enzyme family, can remove the S-palmitoylation from N-RAS, facilitating cancer development. It is involved in multiple pathways, such as the PI3K/AKT signaling pathway, and has significant biological importance in cancer-related processes [1].

In hepatocellular carcinoma (HCC) cells, USP35 can stabilize ABHD17C by inhibiting its ubiquitination, promoting HCC development through activation of the PI3K/AKT pathway. Knockdown of USP35 led to decreased ABHD17C protein level, impaired PI3K/AKT pathway, reduced proliferation, cell cycle arrest, increased apoptosis, and mitigated migration and invasion in HCC cells, and xenograft assay data also supported these in vitro observations [1].

In pancreatic cancer, ABHD17C is a metabolic and immune-related gene signature. It participates in the regulation of the immune microenvironment, reshapes the immunosuppressive microenvironment by down-regulating the pH value, enhances glycolysis, and mediates resistance to anti-PD1 therapy. In vivo experiments showed that its overexpression promoted pancreatic cancer progression [2]. The long non-coding RNA MIR4435-2HG promotes pancreatic cancer progression by regulating ABHD17C through sponging miR-128-3p. Knocking down MIR4435-2HG hindered PC progression by suppressing ABHD17C expression via miR-128-3p upregulation in vitro and in vivo [3].

In conclusion, ABHD17C plays crucial roles in cancer development, especially in HCC and pancreatic cancer. Research on ABHD17C using in vivo models like xenograft assays in HCC and in vivo animal experiments in pancreatic cancer has revealed its functions in promoting cancer cell proliferation, migration, invasion, and its impact on the immune microenvironment and related signaling pathways, providing potential therapeutic targets for these cancers.