Journal
MOLECULAR MEDICINE REPORTS
Volume 11, Issue 1, Pages 571-576Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2014.2675
Keywords
microRNA-143; autophagy-related 2B; microRNA; non-small cell lung cancer; autophagy; glycolysis
Categories
Funding
- National Basic Research Program of China [2011CBA01105]
- National Natural Science Foundation of China [31170750, 31100570]
- Innovation Program of Shanghai Municipal Commission of the Sciences and Technology [11ZR141220]
- State Key Laboratory of Molecular Biology, Institute of Biochemistry and Molecular Biology, Shanghai Institutes of Life Sciences, Chinese Academy of Sciences
Ask authors/readers for more resources
microRNAs (miRNAs) are small, non-coding RNAs involved in multiple biological pathways by regulating post-transcriptional gene expression. Previously, autophagy has been reported to suppress the progression of non-small cell lung cancer (NSCLC). However, how miRNAs regulate autophagy in NSCLC remains to be elucidated. In the present study, the autophagy gene, autophagy-related 2B (ATG2B), was identified as a novel target of miR-143. The overexpression of miR-143 was able to downregulate the expression of atg2b at the transcriptional and translational levels by direct binding to its 3 untranslated region. Cell proliferation was significantly inhibited by the ectopic expression of miR-143 in H1299 cells. Knockdown of ATG2B resulted in a similar phenotype, with the overexpression of miR-143 in NSCLC cells. Furthermore, knockdown of ATG2B and hexokinase 2, a key enzyme in glycolysis and another target of miR-143, co-ordinated to inhibit the proliferation of H1299 cells. The results of the present study demonstrated that miR-143 was a novel and important regulator of autophagy by targeting ATG2B and repression of gene expression in autophagy and high glycolysis had a coordinate effect in H1299 cells. These results suggested that ATG2B may be a new potential therapeutic target for NSCLC. Furthermore, it was implied that interrupting autophagy and glycolysis improves NSCLC therapy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available