ASAP2, also known as ArfGAP with SH3 Domain, Ankyrin Repeat And PH Domain 2, is a gene involved in regulating vesicular transport, cellular migration, and autophagy [4]. It can activate GTPases and promote receptor tyrosine kinase signaling, and is associated with pathways like HGF/c-MET signaling, which is crucial in hepatocellular carcinoma (HCC) progression [1].

Knockdown of ASAP2 in HCC cells significantly impaired cell proliferation, migration, and invasion, but promoted apoptosis, while overexpression had the opposite effects. In vivo, ASAP2 promoted HCC cell growth and lung metastasis [1]. In pancreatic cancer, ASAP2-knockout cells generated with CRISPR-Cas9 technology showed that ASAP2 promoted tumor growth by facilitating cell cycle progression through phosphorylation of epidermal growth factor receptor (EGFR) [3]. In diabetic nephropathy, inhibition of circASAP2 aggravated the disease, promoting inflammation, oxidative stress, and ferroptosis [2].

In conclusion, ASAP2 plays essential roles in various biological processes and disease conditions. Model-based research, especially gene-knockout studies, has revealed its significance in cancer progression, such as in HCC and pancreatic cancer, and in diabetic nephropathy. Understanding ASAP2 provides insights into disease mechanisms and potential therapeutic targets.