Inhba, encoding inhibin subunit beta A, is a member of the transforming growth factor-beta (TGF-β) superfamily. It is involved in the synthesis of inhibin A, activin A and activin AB, and participates in multiple biological processes like cell proliferation, apoptosis, hormone synthesis, and is associated with pathways such as SMAD2/3 signaling, Hippo signaling, and immune-related pathways [3,5,6].

In ovarian cancer, INHBA(+) cancer-associated fibroblasts generate an immunosuppressive tumor microenvironment. Intraperitoneal injection of the Activin A neutralizing antibody in mouse models attenuated tumor progression and infiltration of pro-tumorigenic cells, and downregulation of INHBA in human ovarian CAFs inhibited pro-tumorigenic functions [1]. In esophageal squamous cancer cells, knockdown of IGF2BP1, which stabilizes INHBA mRNA, inhibited cell invasion and migration [2]. In gastric cancer, disrupting the GLI1/INHBA positive feedback loop could inhibit tumorigenesis in vivo [4]. In colon cancer, downregulation of INHBA enhanced 5-FU sensitivity, inhibited cell proliferation, and promoted apoptosis, and INHBA conferred 5-FU chemoresistance through negative regulation of Hippo signaling [6].

In conclusion, Inhba plays crucial roles in various biological functions including cell growth, apoptosis, and hormone regulation. Studies using gene-targeted mouse models and other loss-of-function experiments have revealed its significance in multiple cancer types such as ovarian, esophageal, gastric, and colon cancer, highlighting its potential as a therapeutic target in these diseases.