Hdac7-KO Mouse

HDAC7, a member of the histone deacetylase family, is a "pseudodeacetylase" due to a mutation of a catalytic tyrosine, with its deacetylase-related activities attributed to scaffolding functions [6]. It can participate in multiple cellular pathophysiological processes by exerting deacetylation, and is involved in regulating gene transcription by compacting chromatin as histone deacetylases target histones [2]. HDAC7 is associated with various signaling pathways including β-catenin, PI3K/AKT/mTOR, IKK/NF-κB, and is crucial in processes like cell proliferation, metastasis, and immune responses [1,3,4,8].

In NSCLC, overexpression of HDAC7 promotes cell proliferation and metastasis by upregulating FGF18 via the β-catenin-FGF18 pathway, and deubiquitinase USP10 stabilizes HDAC7 [1]. In ESCC, HDAC7 forms a positive feedback loop with β-catenin and c-Myc to enhance cell growth, and USP10 maintains HDAC7 protein stability [3]. In ovarian cancer, HDAC7 promotes malignancy through the AKT/mTOR signaling pathway [4]. In choroidal melanoma, the HDAC7/c-Myc signaling pathway promotes cell proliferation and metastasis [5]. In glioblastoma, HDAC7 drives the tumor to a mesenchymal-like state via LGALS3-mediated crosstalk between cancer cells and macrophages [7]. In astrocytes, HDAC7 activates the IKK/NF-κB signaling pathway to regulate inflammation [8].

In conclusion, HDAC7 plays essential roles in multiple biological processes and is significantly involved in the development of various cancers and inflammation-related diseases. Studies using different models, though not specifically KO/CKO mouse models in the provided references, have revealed its functions in disease-associated pathways, highlighting its potential as a prognostic biomarker and therapeutic target in these disease areas.