Arhgap30, also known as Rho GTPase-activating protein 30, is a member of the Rho GTPase-activating proteins (Rho GAPs) family. It can enhance the intrinsic hydrolysis of GTP and negatively regulate Rho-GTPase. It is involved in multiple cellular processes such as cytoskeleton organization, cell adhesion, and actin dynamics [6]. It also participates in important signaling pathways like the PI3K/AKT/mTOR, β-catenin, and Wnt/β-catenin pathways, and its dysregulation is associated with various cancers [2,3,7]. Genetic models, especially gene knockout (KO) or conditional knockout (CKO) mouse models, can be valuable for studying its functions.

In colorectal cancer, Arhgap30 binds to p53 C-terminal domain and P300, facilitating P300-mediated acetylation of p53 at lysine 382, which is crucial for p53 functional activation. Low Arhgap30 expression associates with poor survival of CRC patients [1].

In ovarian cancer, knockdown of Arhgap30 suppresses cell proliferation, migration, and invasiveness by inhibiting the PI3K/AKT/mTOR signaling pathway [2].

In pancreatic cancer, overexpression of Arhgap30 attenuates cancer progression by inactivating the β-catenin pathway, while knockdown has the opposite effect [3].

In cervical cancer, overexpression of Arhgap30 suppresses cell growth by downregulating ribosome biogenesis [4].

In lung adenocarcinoma, DNA methylation of Arhgap30 is negatively associated with its expression, reducing tumor immunity and being detrimental to patient survival [5].

In lung cancer, Arhgap30 overexpression impedes cell proliferation, migration, and invasion by inhibiting the Wnt/β-catenin signaling pathway [7]. Also, in lung adenocarcinoma, KIAA1429 regulates cell proliferation and metastasis through the PI3K/AKT pathway by modulating Arhgap30 expression [8].

In colorectal cancer, SRSF3, an oncogene, regulates Arhgap30/Ace-p53, affecting cell proliferation, migration, and survival [9].

In conclusion, Arhgap30 plays essential roles in regulating multiple cellular functions and signaling pathways. Studies using KO/CKO mouse models, or in-vitro loss-of-function experiments, have revealed its significance in various cancer types. These findings contribute to a better understanding of the biological functions of Arhgap30 and provide potential targets for cancer diagnosis, prognosis, and treatment.