Detailed N-glycan analysis combining Glycan profiles taken by Lectin Microarrays and AI

A group from Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA, etc. has reported a lectin and AI-based approach to predict N-glycan structures and determine their relative abundance in purified proteins based on lectin-binding patterns.

This method can be used when the number of glycanss to be evaluated is limited, but there are a lot of problems when applying it generally.

A similar software named “SA/DL easy” had been created by Mx using Deep Learning as a core technology 5 years ago. By using this software, you can quickly do the same thing.
The problem lies in the tedious work of creating training data, or preparing a large number of expressed glycan structures whose structures have been properly identified, and obtaining glycan profiles.

From the roles of galectins in epithelial-to-mesenchymal transition particulary in cancer

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.

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? ?

α2,3-sialylation is essential for melanoma growth and progression

A group from Department of Pathology, NYU Grossman School of Medicine, New York, USA etc. has reported about cganges in glycosylation of melanoma.

It has shown using lectin microarrays that α1,2 fucose decreased in primary melanoma compared to nevi.
Interestingly, core fucose was high in nevi and lower in primary melanoma but then regained in metastatic melanoma.
It was also observed that 2,3 syalylation increased significantly in both primary and metastatic melanoma compared to nevi.