The relationship between Slit3 and tumors

This figure systematically combs the expression regulation mode, core mechanism and biological function of Slit3 in colorectal cancer, gastric cancer, liver cancer, lung cancer, breast cancer, thyroid cancer, malignant melanoma and other tumors. Slit3 is not a single tumor suppressor or promoter, but plays a dual role that is dependent on the type of cancer. In colorectal cancer, gastric cancer, hepatocellular carcinoma, lung adenocarcinoma, and early breast cancer, Slit3 is often down regulated or missing due to methylation or miRNA (such as miR-218) regulation. By removing the inhibition of downstream pathways, Slit3 can activate cell cycle, EMT process, and MMPs expression, thereby promoting tumor proliferation, invasion, metastasis, and chemotherapy resistance; In thyroid cancer, triple negative breast cancer and malignant melanoma, Slit3 overexpression can inhibit tumor growth, induce apoptosis and block metastasis by inhibiting PDGFRA/PLCG1, Wnt/β - catenin, AP-1/MMP axis and other pathways. Overall, the absence or inactivation of Slit3 generally promotes malignant progression of tumors, while restoring its expression or function has anti-cancer potential.