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HIF1A-AS2 promotes the metabolic reprogramming and progression of colorectal cancer via miR-141-3p/FOXC1 axis
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HIF1A-AS2 promotes the metabolic reprogramming and progression of colorectal cancer via miR-141-3p/FOXC1 axis
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HIF1A-AS2 promotes the metabolic reprogramming and progression of colorectal cancer via miR-141-3p/FOXC1 axis
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Journal Article
HIF1A-AS2 promotes the metabolic reprogramming and progression of colorectal cancer via miR-141-3p/FOXC1 axis
2024
Overview
lncRNA can regulate tumorigenesis development and distant metastasis of colorectal cancer (CRC). However, the detailed molecular mechanisms are still largely unknown. Using RNA-sequencing data, RT-qPCR, and FISH assay, we found that HIF1A-AS2 was upregulated in CRC tissues and associated with poor prognosis. Functional experiments were performed to determine the roles of HIF1A-AS2 in tumor progression and we found that HIF1A-AS2 can promote the proliferation, metastasis, and aerobic glycolysis of CRC cells. Mechanistically, HIF1A-AS2 can promote FOXC1 expression by sponging miR-141-3p. SP1 can transcriptionally activate HIF1A-AS2. Further, HIF1A-AS2 can be packaged into exosomes and promote the malignant phenotype of recipient tumor cells. Taken together, we discovered that SP1-induced HIF1A-AS2 can promote the metabolic reprogramming and progression of CRC via miR-141-3p/FOXC1 axis. HIF1A-AS2 is a promising diagnostic marker and treatment target in CRC.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
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/ 13/109
/ 13/51
/ 13/89
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/ 38
/ 38/77
/ 38/90
/ 38/91
/ Animals
/ Biomedical and Life Sciences
/ Cell Proliferation - genetics
/ Cloning
/ Colorectal Neoplasms - genetics
/ Colorectal Neoplasms - metabolism
/ Colorectal Neoplasms - pathology
/ Exosomes
/ Female
/ Forkhead Transcription Factors - genetics
/ Forkhead Transcription Factors - metabolism
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Hypoxia-Inducible Factor 1, alpha Subunit - genetics
/ Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
/ Male
/ Mice
/ Plasmids
/ RNA, Long Noncoding - genetics
/ RNA, Long Noncoding - metabolism
/ Silk
/ Sp1 Transcription Factor - genetics
/ Sp1 Transcription Factor - metabolism
/ Surgery
