ABCC3, also known as MRP3, is a member of the ABCC subfamily within the ATP-Binding Cassette (ABC) transporter family. ABC transporters play a crucial role in the transport of endo-and xenobiotics. ABCC3 is involved in the transport of various substances, including bile acids, and has been associated with multiple biological processes and disease-related pathways [3,4].

In hepatocellular carcinoma (HCC), BRG1 activates ABCC3 transcription, promoting HCC carcinogenesis. ABCC3-silencing in BRG1-overexpressing cells abrogates proliferation and migration, while ABCC3 over-expression rescues these phenotypes in BRG1-depleted cells. High BRG1/ABCC3 expression predicts poor prognosis in HCC patients [1].

In pancreatic ductal adenocarcinoma (PDAC), ABCC3 is overexpressed. Disrupting its function via genetic knockdown reduces pancreatic cancer cell growth in vitro and in vivo, by inhibiting STAT3 and HIF1α signalling pathways [5].

In glioblastoma, ABCC3 expression is associated with poor survival and impaired response to temozolomide, and its high expression is restricted to glioblastoma, making it a suitable target for immunotargeted applications [2].

In colorectal cancer, down-regulation of ABCC3 activates MAPK signalling through the accumulation of deoxycholic acid [4].

In conclusion, ABCC3 is an important transporter involved in multiple disease-related processes. Studies using gene-knockout or knockdown models in various cancer types, such as HCC, PDAC, glioblastoma, and colorectal cancer, have revealed its role in cancer cell proliferation, migration, and response to treatment. These findings suggest that targeting ABCC3 could potentially be a strategy for improving cancer treatment.