The regulatory roles of long non-coding RNAs in the development of chemoresistance in breast cancer
Metrics: PDF 1062 views | HTML 4446 views | ?
Akshay Malhotra1, Manju Jain1, Hridayesh Prakash2, Karen M. Vasquez3 and Aklank Jain4
1Center for Biochemistry and Microbial Sciences, Central University of Punjab, Bathinda, Punjab, India
2Laboratory of Translational Medicine, School of Life Sciences, University of Hyderabad, Gachibowli, Hyderabad, India
3Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Dell Pediatric Research Institute, TX, USA
4Center for Animal Sciences, Central University of Punjab, Bathinda, Punjab, India
Aklank Jain, email: email@example.com
Keywords: breast cancer; chemoresistance; long non-coding RNA; lncRNA; drug resistance
Received: June 06, 2017 Accepted: October 13, 2017 Published: November 08, 2017
Chemoresistance is one of the major hurdles in the treatment of breast cancer, which limits the effect of both targeted and conventional therapies in clinical settings. Therefore, understanding the mechanisms underpinning resistance is paramount for developing strategies to circumvent resistance in breast cancer patients. Several published reports have indicated that lncRNAs play a dynamic role in the regulation of both intrinsic and acquired chemoresistance through a variety of mechanisms that endow cells with a drug-resistant phenotype. Although a number of lncRNAs have been implicated in chemoresistance of breast cancer, their mechanistic roles have not been systematically reviewed. Thus, here we present a detailed review on the latest research findings and discoveries on the mechanisms of acquisition of chemoresistance in breast cancer related to lncRNAs, and how lncRNAs take part in various cancer signalling pathways involved in breast cancer cells. Knowledge obtained from this review could assist in the development of new strategies to avoid or reverse drug resistance in breast cancer chemotherapy.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.