Abstract
Circular RNAs (circRNAs) have gained much attention for their crucial regulatory roles in human diseases and cancers. However, the role and the mechanism of circRNA ArfGAP with FG repeats 1 (circAGFG1) in non-small-cell lung cancer (NSCLC) are still largely unknown. circAGFG1 was highly expressed in NSCLC, and high expression of circAGFG1 was closely related to the low survival rate of NSCLC patients. circAGFG1 knockdown inhibited the proliferation, migration, and invasion and promoted the apoptosis of NSCLC cells. circAGFG1 bound to miR-28-5p in NSCLC cells, and circAGFG1 promoted NSCLC progression partly through sponging miR-28-5p in vitro. HIF-1α was a target of miR-28-5p, and miR-28-5p overexpression-mediated influences in NSCLC cells were partly overturned by the addition of HIF-1α overexpression plasmid. circAGFG1/miR-28-5p/HIF-1α axis regulated cellular glycolytic metabolism in NSCLC cells. circAGFG1 silencing restrained the xenograft tumor growth in vivo. circAGFG1 promoted the proliferation, migration, and invasion and suppressed the apoptosis of NSCLC cells through accelerating the glycolysis via miR-28-5p/HIF-1α axis.
Highlights
Non-small-cell lung cancer (NSCLC) is a common cancer and results in a great burden on the society
We found that circAGFG1 was upregulated in NSCLC
According to the data of the survival curve analysis, we found that high expression of circAGFG1 might be a marker of poor prognosis of NSCLC patients
Summary
Non-small-cell lung cancer (NSCLC) is a common cancer and results in a great burden on the society. MiRNAs are reported to regulate the initiation and the progression of diverse malignancies, including NSCLC. Targeting HIF-1α signaling is an important direction for the treatment of cancers, including gastric cancer and NSCLC [16,17]. We found a novel signal axis of circAGFG1/ miR-28-5p/HIF-1α that was implicated in the regulation of NSCLC development. Cancer cells exhibit a unique metabolic phenotype, termed as the Warburg effect, featured by increased glycolytic metabolism and decreased oxidative phosphorylation, even with the presence of oxygen [18]. The Warburg effect provides growth advantages for cancer cells under the hypoxic tumor microenvironment, and it decreased the release of reactive oxygen species in mitochondria [19,20]. The role and the downstream signal network of circAGFG1 in NSCLC cells were explored.
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