Sulforaphane Targets the TBX15/KIF2C Pathway to Repress Glycolysis and Cell Proliferation in Gastric Carcinoma Cells

AbstractAbstractThe effects of sulforaphane on glycolysis and proliferation of SGC7901 and BGC823 gastric carcinoma cell lines were analyzed, and the potential mediating role of the TBX15/KIF2C axis was explored. SGC7901 and BGC823 cells stably over- or underexpressing TBX15 were exposed to sulforaphane, and cell viability was assessed together with the expression of TBX15, KIF2C, and proteins involved in glycolysis, glucose uptake, and lactate production. Overexpressing TBX15 in SGC7901 and BGC823 cells significantly reduced glucose uptake, lactate production, cell viability, expression of KIF2C, and pyruvate kinase M2-mediated (PKM2) glycolysis. These effects were recapitulated by treatment with sulforaphane. The anti-tumor effects of sulforaphane were antagonized by down-regulation of TBX15, up-regulation of KIF2C or addition of a PKM2 agonist. Sulforaphane can reduce cell proliferation and PKM2-mediated glycolysis in gastric carcinoma cells, apparently by activating the TBX15/KIF2C pathway. AcknowledgmentsThe authors thank Hubei Key Laboratory of Kidney Disease Pathogenesis and Intervention Hubei.Disclosure statementThe authors declare no conflict of interest.Additional informationFundingThe author(s) reported there is no funding associated with the work featured in this article.