Taraxasterol suppresses cell proliferation and boosts cell apoptosis via inhibiting GPD2-mediated glycolysis in gastric cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2021-10-18

AUTHORS

Yang Zhao, Li Zhang, Min Guo, Haixia Yang

ABSTRACT

Gastric cancer (GC) is the most common malignant tumor of digestive tract. Taraxasterol (TAX), a kind of phytosterol, has been proved to exert anti-tumor functions in GC. Herein, the current work was carried out to identify the biological role of TAX and molecular mechanisms underlying TAX in the progression of GC. In the present study, CCK-8 assay, Colony formation assay, EDU staining and TUNEL staining were performed to evaluate the malignant behaviors of GC cells. Levels of proliferation and apoptosis-associated proteins were assessed using western blotting analysis. Besides, GPD2 expression in GC cells was presented on CCLE database and the interaction between TAX and GPD2 was obtained from STRING database. The glucose uptake, lactate production, LDH activity, ATP and expressions of glycolysis-associated enzymes were measured to evaluate glycolysis level. Results of the present research revealed that TAX suppressed the proliferative and clone-forming abilities of GC cells and boosted the apoptosis of GC cells. TAX reduced GPD2 expression in GC cells. Furthermore, overexpression of GPD2 reversed the inhibitory effects of TAX on the proliferative and clone-forming abilities of GC cells as well as abolished the promoting effects of TAX on the apoptosis of GC cells. Besides, upregulation of GPD2 abrogated the inhibition of TAX on glycolysis. To conclude, TAX could suppress GC progression via inhibiting GPD2-mediated glycolysis, which helps to develop a promising molecular target for GC therapies. More... »

PAGES

815-825

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10616-021-00499-8

DOI

http://dx.doi.org/10.1007/s10616-021-00499-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1141966750

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/34776631


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