The Possible Role of the Long Non-coding RNA NORAD in Mitomycin C-Related Chemoresistance

Abstract

Aim:Non-coding ribonucleic acid (RNA) activated by deoxyribonucleic acid (DNA) damage (NORAD) is a long non-coding RNA activated during DNA damage response. Accumulating evidence suggest that NORAD is overexpressed in human cancers and associated with the drug-induced chemoresistance. The present study aims to explore the possible role of long non-coding RNA NORAD during mitomycin C-related chemoresistance and mitomycin C-induced DNA damage response.Materials and Methods:In cell culture experiments, MDA-MB-231 breast cancer cells were used. MTT cell viability assay was used to determine the effects of mitomycin C on breast cancer cells and application dose was determined accordingly. For analysis of NORAD gene expression levels, quantitative real-time polymerase chain reaction method was used.Results:Mitomycin C was found to suppress cell viability of breast cancer cells in a dose-dependent manner and half-maximal inhibitory concentration was determined as 1.12 µg/mL (p<0.0001). Notably, significant differential activation of NORAD was determined in breast cancer cells treated with the mitomycin C (p<0.0001).Conclusion:Findings obtained here strongly suggest that NORAD is possibly involved in mitomycin C-related chemoresistance and mitomycin C-induced DNA damage response.

Keywords

• dna damage
• breast cancer
• mitomycin c
• lncrna
• norad