ArticleAsian Pacific journal of cancer prevention : APJCP2023
Butyrate-mediated Resistance to Trichostatin A Accompanied by Elevated Expression of Glucose Transporter 3 (GLUT3) in Human Colorectal Carcinoma HCT116 Cells.
Article in Asian Pacific journal of cancer prevention : APJCP, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 3 citations in OpenAlex.
- Unveiling the tumor microenvironment in colorectal cancer therapeutic resistance.Frontiers in cell and developmental biology · 2025Review
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2 authors at 2 institutions in 1 country.
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Abstract
objectiveThe aim of study was to investigate the correlation of GLUT3 upregulation and butyrate-mediated acquired chemoresistance.
methodA butyrate-resistant CRC cell model was established from parental (PT) HCT116 cells by gradually increasing the concentration of sodium butyrate (NaBu), followed by evaluation of resistance to butyrate and trichostatin A (TSA) by the MTT method. The expression of SLC2A3 gene and GLUT3 protein were assessed by semi-quantitative RT-PCR and western blotting, respectively. The correlation of GLUT3 and butyrate-induced acquired chemoresistance was investigated using SLC2A3 silencing.
resultsButyrate-resistant (BR) HCT116 cells were more tolerant to butyrate-induced cell death and also resist to 750 and 1000 nM TSA when compared with HCT116-PT cells (p <0.05). Long-term exposure to butyrate revealed that upregulation of the SLC2A3 gene was significantly increased by more than 20 fold (p < 0.01), and that of GLUT3 was elevated by approximately 2 fold (p < 0.05) in HCT116-BR cells. Silencing of the SLC2A3 gene increased the sensitivity of HCT116-BR cells to the effects of TSA.
conclusionUpregulation of GLUT3 is associated with resistance to butyrate and TSA. GLUT3 is a molecular target for the detection of chemoresistant CRC cells and thus a potential target for diagnostic strategies.
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