I have read a review article on the epithelial-to-mesenchymal transition (EMT) of galectins written by the groups of CEBICEM, Facultad de Medicina y Ciencia, Universidad San Sebastián, Santiago, Chile, and others. The following is the typical phrases extracted from this review.
https://biolres.biomedcentral.com/articles/10.1186/s40659-024-00490-5
In gastric cancer, increased levels of Gal-1 have been associated with lower overall and disease-free survival, as well as with an increased incidence of lymph node metastasis in patients. Gastric cancer cell lines produce Gal-1, which promotes EMT and increases proliferation, invasion and metastatic potential of these cells. In ovarian cancer, serum samples show that Gal-1 levels are increased and correlate with a higher histological grade and lymph node metastasis. In ovarian cancer cell lines, Gal-1 overexpression promotes EMT and increases cell migration and invasion through the activation of the MAPK-JNK/p38 signaling pathway, while silencing of Gal-1 has opposite effects. High levels of Gal-1 are detected in stromal cells from gastric cancer and pancreatic ductal adenocarcinoma tumors in correlation with an EMT phenotype of carcinoma cells. Gal-1-overexpression in pancreatic stellate cells (PSC) induces EMT in co-cultured pancreatic carcinoma cells, enhancing their proliferation and invasion through the NF-κB pathway. Downregulation of Gal-3 expression reduces tumor growth in xenograft colon cancer models whereas its overexpression enhances the metastatic potential of cancer cells. In breast, colon, and prostate cancer cell lines exogenously added Gal-3 promotes EMT by its interaction with Trop-2, a highly-glycosylated membrane protein involved in cancer progression. Gal-4 has been reported in human prostate cancer tissues with expression levels correlating with metastasis and poor patient survival. Gal-8 is a widely expressed galectin in human tissues and carcinomas and has been associated with an unfavorable prognosis in various types of cancer. Gal-8 contributes to cancer progression and metastasis by regulating the production of immunoregulatory cytokines, thereby facilitating the recruitment of cancer cells to metastatic sites.
In other words, different types of galectins are involved in cancer in various places, but I think the issue is the degree of the contribution of galectin involvement. Glycans and lectins basically play regulatory roles except for innate immunity and congenital disorder of glycosylation (CDG).
Therefore, when trying to cure disease from a view point of glycans and lectins, I think it is necessary to narrow down the disease to those in which these are involved with higher contributions.
What do you think? ?