Abstract
Lung adenocarcinoma (LUAD) has long been one of the predominant reasons for the global cancer-linked mortality. The tumor progression is shown by several studies to be promoted by increased glycolysis. Enolase 1 (ENO1), as a glycolysis enzyme, performs pivotal role in glucose metabolism and contributes to tumor progression of numerous cancers. Circular RNAs (circRNAs) are catching increasing attentions for their surging roles in regulating gene expression in cancers. Our work is to uncover the regulatory mechanism circ-ENO1 on its host gene ENO1 and its function in glycolysis and tumor progression. Circ-ENO1 and its host gene ENO1 were identified to be upregulated in LUAD cells. Functionally, silencing circ-ENO1 retarded glycolysis, inhibited proliferation, migration and EMT, induced apoptosis. The cytoplasmic localization of circ-ENO1 was determined by FISH and subcellular fractionation. Mechanistically, circ-ENO1 acted as a ceRNA to interact with miR-22-3p and upregulate ENO1 expression. In vivo experiments certified that circ-ENO1 drove tumor growth and metastasis in vivo. In summary, current study elucidated that circ-ENO1 promoted glycolysis and tumor progression in LUAD by miR-22-3p/ENO1 axis, indicating circ-ENO1 as a promising treatment target for LUAD patients.
Highlights
Lung cancer is known to be a major contributor of global tumor-related deaths, the worldwide 5-year survival rate of which is around 16.6%1,2
We revealed through PCR that circ-Enolase 1 (ENO1) amplified by divergent primers was detectable in cDNA rather than genomic DNA, which confirmed that circ-ENO1 was a bona fide circRNA (Fig. 1e)
These results suggested that circ-ENO1 was a bone fide circRNA upregulated in Lung adenocarcinoma (LUAD)
Summary
Lung cancer is known to be a major contributor of global tumor-related deaths, the worldwide 5-year survival rate of which is around 16.6%1,2. Recent years have witnessed the advancement of clinical and experimental oncology for lung cancer, the prognosis of LUAD patients sees no dramatic rise[4]. Improving the understanding of mechanisms behind tumor progression and tumor metastasis in lung cancer is imminently required. CircRNAs can function through competing endogenous RNA (ceRNAs) network, competitively targeting certain miRNAs to upregulate mRNAs7,8. The roles of circRNAs in promoting tumor progression have been largely revealed in a diversity of cancers[9,10,11], including lung cancer[11,12]. We identified a new circRNA, circ-0000013, upregulated in LUAD through circRNA sequencing. No study has explored circ-0000013 in cancers yet
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