RNF180, an important member of the E3 ubiquitin ligase family, is considered a tumor suppressor gene. It is involved in multiple cellular processes such as cell development, proliferation, and apoptosis. In signaling pathways, RNF180 has been linked to regulating the STAT3 pathway via RhoC in gastric cancer cells, and it may also participate in other pathways related to tumorigenesis and inflammation [2].

In colorectal cancer, RNF180 overexpression inhibits cell viability and induces apoptosis, while its depletion enhances cell survival. It ubiquitinates WISP1, a critical downstream molecule, leading to WISP1 downregulation and suppression of tumor growth in patient-derived xenograft mouse models.

In gastric cancer, RNF180 can inhibit cell proliferation, invasion, and migration. It reduces STAT3 phosphorylation by promoting the ubiquitination and degradation of RhoC. Additionally, RNF180 can prevent excessive PCDH10 methylation by promoting ubiquitination of DNMT1, thus suppressing gastric cancer cell proliferation and metastasis.

In triple-negative breast cancer, RNF180 degrades RAD51 by ubiquitination, inhibiting cell growth, metastasis, and sensitizing cells to Gefitinib.

In ovarian cancer, RNF180 impairs the IPO4/SOX2 complex stability, inhibits SOX2-mediated malignancy, and suppresses the progression of ovarian cancer [1,2,3,4,5].

In conclusion, RNF180 plays a crucial role in suppressing tumor growth and development through various mechanisms, mainly by ubiquitinating key downstream molecules. Studies using different models, including patient-derived xenograft mouse models, have revealed its significance in cancers such as colorectal, gastric, triple-negative breast, and ovarian cancers. These findings provide potential therapeutic targets for these diseases.