Journal
CANCERS
Volume 14, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/cancers14092101
Keywords
MDR; lncRNA; breast cancer; chemoresistance; chemotherapy; exosome
Categories
Funding
- National Natural Science Foundation of China [21877084, 21671150, 81860547, 82073387]
- Shanghai Pudong New Area Health and Family Planning Commission Leading Talent Training Program [PWRI2019-07]
- Shanghai Pudong New Area Science and Technology Development Fund, Innovation Fund [PKJ2017-Y18]
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This article systematically summarizes the role of long noncoding RNAs (lncRNAs) in multidrug resistance (MDR) of breast cancer. The mechanisms of lncRNA-mediated MDR, including apoptosis, autophagy, DNA repair, cell cycle, drug efflux, epithelial-mesenchymal transition, epigenetic modification and the tumor microenvironment, are elaborated. It is suggested that lncRNAs may serve as promising prognostic biomarkers and therapeutic targets for breast cancer patients receiving chemotherapy.
Simple Summary Multidrug resistance (MDR) is a major cause of breast cancer (BC) chemotherapy failure. Long noncoding RNAs (lncRNAs) have been shown closely related to the chemoresistance of BC. In this work, the mechanisms of lncRNA-mediated MDR in BC were elaborated from eight sections, including apoptosis, autophagy, DNA repair, cell cycle, drug efflux, epithelial-mesenchymal transition, epigenetic modification and the tumor microenvironment. Additionally, we also discuss the clinical significance of lncRNAs, which may be biomarkers for diagnosis, therapy and prognosis. Breast cancer (BC) is a highly heterogeneous disease and presents a great threat to female health worldwide. Chemotherapy is one of the predominant strategies for the treatment of BC; however, multidrug resistance (MDR) has seriously affected or hindered the effect of chemotherapy. Recently, a growing number of studies have indicated that lncRNAs play vital and varied roles in BC chemoresistance, including apoptosis, autophagy, DNA repair, cell cycle, drug efflux, epithelial-mesenchymal transition (EMT), epigenetic modification and the tumor microenvironment (TME). Although thousands of lncRNAs have been implicated in the chemoresistance of BC, a systematic review of their regulatory mechanisms remains to be performed. In this review, we systematically summarized the mechanisms of MDR and the functions of lncRNAs mediated in the chemoresistance of BC from the latest literature. These findings significantly enhance the current understanding of lncRNAs and suggest that they may be promising prognostic biomarkers for BC patients receiving chemotherapy, as well as therapeutic targets to prevent or reverse chemoresistance.
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