Acvr2a, also known as activin receptor type 2A, is a key component in multiple signaling pathways. It is involved in the activin-A signaling pathway and plays a role in regulating biological processes such as endometrial receptivity and embryo implantation through the ACVR2A-SMAD1/SMAD5 axis [2]. It may also be part of the TGF-β pathway, which is related to the pathogenesis of some cancers [5].

In endometrial receptivity, conditional deletion of Acvr2a in mice using progesterone receptor-cre (PR-cre) demonstrated that BMP signaling occurs via ACVR2A during embryo implantation, and ACVR2B is dispensable [2]. In hepatocellular carcinoma, circACVR2A (hsa_circ_0001073) promotes the proliferation, migration, and invasion of HCC cells by acting as a miRNA sponge for miR-511-5p, regulating the PI3K-Akt signaling pathway [1]. Also, in NASH-related HCC, ACVR2A mutation rates are higher compared to other HCC aetiologies, and in vitro, ACVR2A silencing promotes cell proliferation [3]. In colon cancer, the activin A/ACVR2A axis inhibits epithelial-to-mesenchymal transition and cell migration and invasion by activating SMAD2 [4].

In conclusion, Acvr2a is crucial in biological processes like embryo implantation and is significantly associated with multiple cancers. Gene knockout or conditional knockout mouse models have been instrumental in revealing its role in endometrial function and cancer-related processes, providing valuable insights into disease mechanisms and potential therapeutic targets.