Far upstream element -binding protein 1 (FUBP1) participates in the malignant process and glycolysis of colon cancer cells by combining with c-Myc

Human distal upstream element (Fuse) binding protein 1 (FUBP1) is a transcriptional regulator of c-Myc and represents an important prognostic marker in many cancers. Therefore, the present study aimed to investigate whether FUBP1 could combine with c-Myc to participate in the progression of colon ca...

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Bibliographic Details
Published in:Bioengineered 2022-05, Vol.13 (5), p.12115-12126
Main Authors: Wang, Shanwei, Wang, Yanli, Li, Sheng, Nian, Shen, Xu, Wenjing, Liang, Fenli
Format: Article
Language:English
Subjects:
c-myc
Cell Line, Tumor
Cell Proliferation - genetics
colon cancer
Colonic Neoplasms - genetics
DNA-Binding Proteins - genetics
FUBP1
Gene Expression Regulation, Neoplastic
glycolysis
Glycolysis - genetics
Humans
Lactic Acid
RNA-Binding Proteins - genetics
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Summary:Human distal upstream element (Fuse) binding protein 1 (FUBP1) is a transcriptional regulator of c-Myc and represents an important prognostic marker in many cancers. Therefore, the present study aimed to investigate whether FUBP1 could combine with c-Myc to participate in the progression of colon cancer. Detection of FUBP1 expression was done through reverse transcription-quantitative PCR (RT-qPCR), and the combination of FUBP1 and c-Myc was detected by immunoprecipitation assay. Cell counting kit (CCK)-8, colony formation, transwell and wound healing were applied for assessing the ability of cells to proliferate, migrate, and invade; glycolysis and lactic acid detection kits were used to detect glucose uptake and lactic acid content, while western blotting was adopted to detect the protein expression of glycolysis-related genes. FUBP1 expression was elevated in HCT116 cells relative to other colon cancer cell lines, and silencing FUBP1 could inhibit the ability of HCT116 cells to proliferate, migrate, invade and glycolysis, and enhance its apoptosis. In addition, the results of immunoprecipitation experiments showed that FUBP1 could bind to c-Myc. c-Myc overexpression reversed the inhibitory effects of FUBP1 knockdown on the ability of HCT116 cells to proliferate, migrate, invade and glycolysis. The results indicated that FUBP1 could participate in the deterioration process of colon cancer cells by combining with c-Myc, and it has clinical significance for understanding the key role of FUBP1 in tumor genesis.
ISSN:2165-5979
2165-5987
DOI:10.1080/21655979.2022.2073115