Itga7, short for Integrin Subunit Alpha 7, is a transmembrane receptor belonging to the integrin family. Integrins play crucial roles in cell-matrix and cell-cell adhesion, as well as in signal transduction pathways that regulate various cellular processes such as cell survival, proliferation, and differentiation [1,2,3,4,5,6,7,8,9,10].

In cancer research, loss-of-function studies have shown significant impacts. In ovarian cancer, ITGA7 loss drives the differentiation of adipose-derived mesenchymal stem cells (ADSCs) to cancer-associated fibroblasts (CAFs), which contribute to a tumor-supportive niche [1]. In colorectal cancer, promoter hypermethylation-induced downregulation of ITGA7 promotes cell proliferation and migration by activating the PI3K/AKT/NF-κB pathway [8]. In breast cancer, knocking down ITGA7 significantly inhibits cell migration and invasion [10]. In cervical cancer, high ITGA7 expression is linked with poor differentiation, lymph node metastasis, and worse survival [4]. In Ph-acute lymphoblastic leukemia, elevated ITGA7 expression is associated with CNS leukemia occurrence, higher bone marrow blasts, lower complete remission rate, and worse prognosis [5]. In Parkinson's disease models, decreased ITGA7 levels are associated with increased α-synuclein levels, suggesting a role in the disease pathology [7,9].

In conclusion, Itga7 has diverse functions in normal biological processes related to cell adhesion and signaling. Through gene knockout or knockdown studies in various disease models, it has been revealed that Itga7 plays important roles in cancer progression, including metastasis and cell differentiation, as well as in Parkinson's disease pathology. Understanding the function of Itga7 provides insights into the mechanisms of these diseases, potentially leading to new therapeutic strategies.