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Lectin affinity chromatography and quantitative proteomic analysis reveal that galectin-3 is associated with metastasis in nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC) is a serious cancer in East and Southeast Asia. Patients are often diagnosed at advanced stages, rendering treatment failure due to high potential of metastasis. This study identified lectin-binding glycoproteins with a potential role in NPC metastasis. Cell lysate and...

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Detalles Bibliográficos
Autores principales: Aimjongjun, Sathid, Reamtong, Onrapak, Janvilisri, Tavan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7536187/
https://www.ncbi.nlm.nih.gov/pubmed/33020562
http://dx.doi.org/10.1038/s41598-020-73498-y
Descripción
Sumario:Nasopharyngeal carcinoma (NPC) is a serious cancer in East and Southeast Asia. Patients are often diagnosed at advanced stages, rendering treatment failure due to high potential of metastasis. This study identified lectin-binding glycoproteins with a potential role in NPC metastasis. Cell lysate and culture medium in highly metastatic 5-8F, and lowly-metastatic 6-10B NPC cell lines were fractionated by ConA- and WGA-affinity chromatography, and subjected to GeLC-MS/MS. A total of 232 and 197 proteins were identified in ConA-enriched fraction of 5-8F and 6-10B cell lysates respectively. In WGA-enriched fraction, 65 and 164 proteins were found in 5-8F and 6-10B cell lysates respectively. Proteins identified in culture medium for both cell lines were 223 and 85 for ConA-enriched fraction, and 94 and 124 for WGA-enriched fraction from 5-8F and 6-10B respectively. Differentially expressed proteins were functionally categorized into cell–cell adhesion, extracellular matrix, glycolysis, protein homeostasis and/or glycosylation enzymes, and lipid metabolism. Interestingly, Galectin-3 (Gal-3) was highly expressed in 5-8F cells but was lowly expressed in 6-10B cells. The Gal-3 knockdown in 5-8F cells, Gal-3 overexpression in 6-10B cells and treatment with Gal-3 inhibitor revealed that Gal-3 was responsible for metastatic phenotypes including adhesion, migration and invasion. So Galectin-3 may serve as a potential target for NPC therapeutic interventions.