Jing Zhang,1,* Le Wu,1,* Chenchen Wang,2,* Xin Xie,1 Yuying Han1– 3 

1Laboratory of Tissue Engineering, Faculty of Life Science, Northwest University, Xi’an, Shaanxi, People’s Republic of China; 2Department of Critical Care Medicine, the 940th Hospital of Joint Logistics Support Force of PLA, Lanzhou, Gansu, People’s Republic of China; 3Science and Education Department, Xi’an No. 5 Hospital, Xi’an, Shaanxi, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Yuying Han; Xin Xie, Laboratory of Tissue Engineering, Faculty of Life Science, Northwest University, 229 Taibai North Road, Xi’an, Shaanxi, 710069, People’s Republic of China, Email hanyuying@nwu.edu.cn; xiexin@nwu.edu.cn

Abstract: In the past few decades, chemotherapy has been one of the most effective cancer treatment options. Drug resistance is currently one of the greatest obstacles to effective cancer treatment. Even though drug resistance mechanisms have been extensively investigated, they have not been fully elucidated. Recent genome-wide investigations have revealed the existence of a substantial quantity of long non-coding RNAs (lncRNAs) transcribed from the human genome, which actively participate in numerous biological processes, such as transcription, splicing, epigenetics, the cell cycle, cell differentiation, development, pluripotency, immune microenvironment. The abnormal expression of lncRNA is considered a contributing factor to the drug resistance. Furthermore, drug resistance may be influenced by genetic and epigenetic variations, as well as individual differences in patient treatment response, attributable to polymorphisms in metabolic enzyme genes. This review focuses on the mechanism of lncRNAs resistance to target drugs in the study of tumors with high mortality, aiming to establish a theoretical foundation for targeted therapy.

Keywords: lncRNA, drug resistance, chemotherapy, tumor, immune escape