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Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas

  
@article{JTD34847,
	author = {Yinbin Zheng and Yi Chen and Hongjing Jiang and Hongdian Zhang and Hua Wang and Jun Xu and Zhentao Yu},
	title = {Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas},
	journal = {Journal of Thoracic Disease},
	volume = {12},
	number = {2},
	year = {2020},
	keywords = {},
	abstract = {Background: CirRNA Circ_0058063 has been proven as an oncogene in bladder cancer, while its involvement in esophageal squamous-cell carcinomas (ESCC) is unknown. This study aimed to investigate the role of Circ_0058063 in ESCC.
Methods: Paired ESCC and non-tumor tissues were collected from ESCC patients and gene expression was analyzed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Gene interactions were analyzed by overexpression experiment. Glucose uptake was analyzed by glucose uptake assay. Cell proliferation was analyzed by cell proliferation assay.
Results: We found that Circ_0058063 was upregulated in ESCC and positively correlated with GLUT1 mRNA. It is known that GLUT1 plays critical roles in glucose transportation and glucose supports the Warburg Effect as the major metabolic precursor. In ESCC cells, Circ_0058063 and GLUT1 overexpression both promoted glucose uptake. In ECSS cells, Circ_0058063 overexpression resulted in the upregulated, while Circ_0058063 knockdown resulted in downregulated GLUT1. In cell proliferation assay, Circ_0058063 and GLUT1 overexpression resulted in the increased, while Circ_0058063 knockdown resulted in the decreased rate of ESCC cell proliferation. Moreover, GLUT1 overexpression reduced the effects of Circ_0058063 knockdown.
Conclusions: Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in ESCC to promote cell proliferation.},
	issn = {2077-6624},	url = {http://jtd.amegroups.com/article/view/34847}
}