https://www.ncbi.nlm.nih.gov/gene/56667
2015 : https://www.ncbi.nlm.nih.gov/pubmed/25672256/
Oncogenesis. 2018 Feb 22;7(2):19. doi: 10.1038/s41389-018-0031-0.
MUC13 contributes to rewiring of glucose metabolism in pancreatic cancer.- DRCC1; MUC-13
- Summary
- Epithelial mucins, such as MUC13, are a family of secreted and cell surface glycoproteins expressed by ductal and glandular epithelial tissues (Williams et al., 2001 [PubMed 11278439]).[supplied by OMIM, Jul 2008]
- Expression
- Biased expression in duodenum (RPKM 317.3), small intestine (RPKM 271.9) and 4 other tissues
- Protein: Preferred Names
- mucin-13
- Names
- down-regulated in colon cancer 1
- mucin 13, epithelial transmembrane
- https://www.ncbi.nlm.nih.gov/protein/NP_149038.3
2015 : https://www.ncbi.nlm.nih.gov/pubmed/25672256/
Oncogenesis. 2018 Feb 22;7(2):19. doi: 10.1038/s41389-018-0031-0.
Abstract
Pancreatic
tumors are rewired for high-glucose metabolism and typically present
with exceptionally poor prognosis. Recently, we have shown that MUC13,
which is highly expressed in pancreatic tumors, promotes tumor
progression via modulation of HER2 receptor tyrosine kinase activity.
Herein, we investigate a novel, MUC13-mediated molecular mechanism responsible for higher glucose metabolism in pancreatic tumors. Our results demonstrate that MUC13
expression leads to the activation/nuclear translocation of NF-κB p65
and phosphorylation of IκB, which in turn upregulates the expression of
important proteins (Glut-1, c-Myc, and Bcl-2) that are involved in
glucose metabolism. MUC13
functionally interacts and stabilizes Glut-1 to instigate downstream
events responsible for higher glucose uptake in pancreatic cancer cells.
Altered MUC13 expression by overexpression and knockdown techniques effectively modulated glucose uptake, lactate secretion, and metastatic phenotypes in pancreatic cancer cells. NF-κB inhibitor, Sulfasalazine, abrogates the MUC13 and Glut-1 interaction, and attenuates events associated with MUC13-induced glucose metabolism. Pancreatic ductal adenocarcinoma (PDAC) patient tissue samples also show a positive correlation between the expression of these two proteins. These results delineate how MUC13 rewire aberrant glucose metabolism to enhance aggressiveness of pancreatic cancer and revealed a novel mechanism to develop newer therapeutic strategies for this exceptionally difficult cancer.
Altered MUC13 expression by overexpression and knockdown techniques effectively modulated glucose uptake, lactate secretion, and metastatic phenotypes in pancreatic cancer cells. NF-κB inhibitor, Sulfasalazine, abrogates the MUC13 and Glut-1 interaction, and attenuates events associated with MUC13-induced glucose metabolism. Pancreatic ductal adenocarcinoma (PDAC) patient tissue samples also show a positive correlation between the expression of these two proteins. These results delineate how MUC13 rewire aberrant glucose metabolism to enhance aggressiveness of pancreatic cancer and revealed a novel mechanism to develop newer therapeutic strategies for this exceptionally difficult cancer.
- PMID: 29467405
- PMCID:PMC5833644
- DOI:10.1038/s41389-018-0031-0
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