Overexpression of microRNA-133b sensitizes non-small cell lung cancer cells to irradiation through the inhibition of glycolysis.

Abstract

Non-small cell lung cancer (NSCLC) accounts for 85% of all types of lung cancer and is the leading cause of world-wide cancer-associated mortalities. Radiation therapy has long been regarded as a fundamental therapeutic treatment strategy for NSCLC. However, alternative therapies for NSCLC remain insufficient, with the majority of cancers developing a high incidence of radioresistance. MicroRNAs (miRNAs/miRs) are endogenous oligonucleotide RNAs that serve an important role in carcinogenesis and tumor progression. In the present study, a novel function of miR-133b that is associated with the radiosensitivity of lung cancer cells is reported. miR-133 was downregulated in radioresistant lung cancer cells, which exhibited an elevated glycolysis rate when compared with radiosensitive cells. Additionally, it was observed that pyruvate kinase isoform M2 (PKM2) is a target of miR-133b, and that the expression of PKM2 is positively correlated with radioresistance. Finally, it was demonstrated that overexpression of miR-133b resensitizes radioresistant lung cancer cells through the inhibition of PKM2-mediated glycolysis. The current study may indicate a novel function of miR-133b, potentially aiding the development of anticancer therapeutics.