Involvement of glucose on TGF-β<sub>1</sub>-induced epithelial-mesenchymal transition in epithelial keratinocytes

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  • 上皮ケラチノサイトにおけるTGF-β<sub>1</sub>誘導性上皮間葉転換に対するグルコースの関与

Abstract

<p>Epithelial-to-mesenchymal transition (EMT) is a unique program in which epithelial cells become more like mesenchymal cells. EMT is involved in several processes, including development, wound healing, fibrosis, and cancer progression, but the molecular mechanism remains to be elucidated.</p><p>We analyzed the involvement of glucose on transforming growth factor (TGF)-β1-induced EMT in human keratinocyte HaCaT cells. Using fluorescent staining, TGF-β1-treated HaCaT showed the formation of actin stress fiber, regardless of glucose concentration. EMT-related markers were partially suppressed in TGF-β1-treated cells under low-glucose conditions. Furthermore, both intracellular glucose and lactate, a glucose metabolite, were decreased under low-glucose conditions. We focused on the relationship between autophagy and the partial suppression of EMT under low-glucose conditions because we found in a previous study that LC-3 and GABARAPL1, autophagy markers, may be associated with TGF-β1-induced EMT. The expression of those markers were regulated in a glucose- and TGF-β1-dependent manner.</p><p>Therefore, it is likely that TGF-β1-induced EMT is regulated by glucose-induced autophagy in epithelial keratinocytes.</p>

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