HDAC7, a member of the histone deacetylase family, is a "pseudodeacetylase" due to mutation of a catalytic tyrosine, and its functions are attributed to scaffolding roles [7]. It is involved in multiple cellular pathophysiological processes, and can activate relevant signaling pathways by exerting deacetylation [2].

In cancer research, HDAC7 has been shown to promote the progression of various tumors. In NSCLC, it promotes proliferation and metastasis via stabilization by deubiquitinase USP10 and activation of the β -catenin-FGF18 pathway [1]. In ESCC, HDAC7 forms a positive feedback loop with β -catenin and c-Myc, and its protein stability is maintained by USP10 to enhance cell growth [3]. In ovarian cancer, HDAC7 promotes malignancy through the AKT/mTOR signalling pathway [6]. In choroidal melanoma cells, the HDAC7/c-Myc signaling pathway promotes cell proliferation and metastasis [9]. Also, in DLBCL, HDAC7 expression is associated with prognosis and immune infiltration [4].

In addition to cancer, in macrophages, HDAC7 acts as an immunometabolic switch, triaging danger signals for appropriate immune responses [5]. In astrocytes, HDAC7 activates the IKK/NF-κB signaling to regulate inflammation [8].

In conclusion, HDAC7 is involved in diverse biological processes, especially playing crucial roles in cancer progression, immune responses, and inflammation. Research on HDAC7 using various models helps to understand its functions and provides potential therapeutic targets for related diseases.