TAF15, also known as TATA-binding protein-associated factor 2N, is a DNA and RNA binding protein involved in crucial biological processes. It participates in inflammatory signalling pathways [1], and is part of the FUS-Ewing sarcoma-TAF15 family [3].

In non-alcoholic steatohepatitis (NASH), hepatocyte-specific knockdown of TAF15 in mice inhibited steatosis, inflammation and fibrosis, while overexpression promoted NASH phenotypes. TAF15 bound to the promoter region of FASN to promote steatosis and interacted with p65 to activate the NF-κB signalling pathway [1].

In lung adenocarcinoma, TAF15 accelerates epithelial-mesenchymal transition (EMT) and metastasis. Knockdown of TAF15 could potentially inhibit these processes as TIF1γ binds to TBP in competition with TAF15 and impedes TAF15/TBP-mediated interleukin 6 (IL-6) transactivation [2].

In gastric cancer, TAF15 knockdown suppressed cell proliferation, migration, invasion in vitro and tumour growth in vivo, with reduced phosphorylation levels of RAF1, MEK and ERK1/2 in cell lines [4].

In conclusion, TAF15 plays significant roles in multiple disease conditions including NASH, lung adenocarcinoma and gastric cancer. Studies using gene knockdown in mouse models have revealed its involvement in regulating lipid metabolism, inflammation, EMT, metastasis and cell proliferation through various signalling pathways. These findings contribute to understanding the disease mechanisms and potentially developing targeted therapies for these diseases.