{"id":14488,"date":"2024-04-06T08:24:09","date_gmt":"2024-04-05T23:24:09","guid":{"rendered":"https:\/\/www.emukk.com\/WP\/?p=14488"},"modified":"2024-04-06T13:02:17","modified_gmt":"2024-04-06T04:02:17","slug":"from-the-role-of-galectins-in-epithelial-to-mesenchymal-transition-particulary-in-cancer","status":"publish","type":"post","link":"https:\/\/www.emukk.com\/WP\/en\/from-the-role-of-galectins-in-epithelial-to-mesenchymal-transition-particulary-in-cancer\/","title":{"rendered":"From the roles of galectins in epithelial-to-mesenchymal transition particulary in cancer"},"content":{"rendered":"

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 Sebasti\u00e1n, Santiago, Chile, and others. The following is the typical phrases extracted from this review.
\nhttps:\/\/biolres.biomedcentral.com\/articles\/10.1186\/s40659-024-00490-5<\/a><\/p>\n

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-\u03baB 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.<\/p>\n

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).<\/p>\n

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.
\nWhat do you think? ?<\/p>\n","protected":false},"excerpt":{"rendered":"

I have read a review article on the epithelial-to-mesenchymal transition (EMT) of galectins written by the gro<\/p><\/div>\n

\u7d9a\u304d\u3092\u8aad\u3080<\/a><\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[70],"tags":[],"class_list":["post-14488","post","type-post","status-publish","format-standard","hentry","category-nature-en"],"aioseo_notices":[],"aioseo_head":"\n\t\t\n\t\n\t\n\t\n\t\n\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t\n\t\t