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Article: GLUT3 induced by AMPK/CREB1 axis is key for withstanding energy stress and augments the efficacy of current colorectal cancer therapies

TitleGLUT3 induced by AMPK/CREB1 axis is key for withstanding energy stress and augments the efficacy of current colorectal cancer therapies
Authors
Issue Date2020
Citation
Signal Transduction and Targeted Therapy, 2020, v. 5, n. 1, article no. 177 How to Cite?
AbstractCancer cells are usually characterized by hyperactive glucose metabolism, which can often lead to glucose scarcity; thus, alternative pathways to rewire cancer metabolism are required. Here, we demonstrated that GLUT3 was highly expressed in colorectal cancer (CRC) and negatively linked to CRC patient outcomes, whereas GLUT1 was not associated with CRC prognosis. Under glucose-limiting conditions, GLUT3 expedited CRC cell growth by accelerating glucose input and fuelling nucleotide synthesis. Notably, GLUT3 had a greater impact on cell growth than GLUT1 under glucose-limiting stress. Mechanistically, low-glucose stress dramatically upregulated GLUT3 via the AMPK/CREB1 pathway. Furthermore, high GLUT3 expression remarkably increased the sensitivity of CRC cells to treatment with vitamin C and vitamin C-containing regimens. Together, the results of this study highlight the importance of the AMPK/CREB1/GLUT3 pathway for CRC cells to withstand glucose-limiting stress and underscore the therapeutic potential of vitamin C in CRC with high GLUT3 expression.
Persistent Identifierhttp://hdl.handle.net/10722/342748
ISSN
2023 Impact Factor: 40.8
2023 SCImago Journal Rankings: 8.737
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDai, Weixing-
dc.contributor.authorXu, Ye-
dc.contributor.authorMo, Shaobo-
dc.contributor.authorLi, Qingguo-
dc.contributor.authorYu, Jun-
dc.contributor.authorWang, Renjie-
dc.contributor.authorMa, Yanlei-
dc.contributor.authorNi, Yan-
dc.contributor.authorXiang, Wenqiang-
dc.contributor.authorHan, Lingyu-
dc.contributor.authorZhang, Long-
dc.contributor.authorCai, Sanjun-
dc.contributor.authorQin, Jun-
dc.contributor.authorChen, Wen Lian-
dc.contributor.authorJia, Wei-
dc.contributor.authorCai, Guoxiang-
dc.date.accessioned2024-04-17T07:05:58Z-
dc.date.available2024-04-17T07:05:58Z-
dc.date.issued2020-
dc.identifier.citationSignal Transduction and Targeted Therapy, 2020, v. 5, n. 1, article no. 177-
dc.identifier.issn2095-9907-
dc.identifier.urihttp://hdl.handle.net/10722/342748-
dc.description.abstractCancer cells are usually characterized by hyperactive glucose metabolism, which can often lead to glucose scarcity; thus, alternative pathways to rewire cancer metabolism are required. Here, we demonstrated that GLUT3 was highly expressed in colorectal cancer (CRC) and negatively linked to CRC patient outcomes, whereas GLUT1 was not associated with CRC prognosis. Under glucose-limiting conditions, GLUT3 expedited CRC cell growth by accelerating glucose input and fuelling nucleotide synthesis. Notably, GLUT3 had a greater impact on cell growth than GLUT1 under glucose-limiting stress. Mechanistically, low-glucose stress dramatically upregulated GLUT3 via the AMPK/CREB1 pathway. Furthermore, high GLUT3 expression remarkably increased the sensitivity of CRC cells to treatment with vitamin C and vitamin C-containing regimens. Together, the results of this study highlight the importance of the AMPK/CREB1/GLUT3 pathway for CRC cells to withstand glucose-limiting stress and underscore the therapeutic potential of vitamin C in CRC with high GLUT3 expression.-
dc.languageeng-
dc.relation.ispartofSignal Transduction and Targeted Therapy-
dc.titleGLUT3 induced by AMPK/CREB1 axis is key for withstanding energy stress and augments the efficacy of current colorectal cancer therapies-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/s41392-020-00220-9-
dc.identifier.pmid32873793-
dc.identifier.scopuseid_2-s2.0-85090026092-
dc.identifier.volume5-
dc.identifier.issue1-
dc.identifier.spagearticle no. 177-
dc.identifier.epagearticle no. 177-
dc.identifier.eissn2059-3635-
dc.identifier.isiWOS:000565207800001-

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