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Abstract
Radiotherapy is one of the main modalities of cancer treatment. However, tumor recurrence following radiotherapy occurs in many cancer patients. A key to solving this problem is the optimization of radiosensitivity. In recent years, long non-coding RNAs (lncRNAs), which affect the occurrence and development of tumors through a variety of mechanisms, have become a popular research topic. LncRNAs have been found to influence radiosensitivity by regulating various mechanisms, including DNA damage repair, cell cycle arrest, apoptosis, cancer stem cells regulation, epithelial–mesenchymal transition, and autophagy. LncRNAs are expected to become a potential therapeutic target for radiotherapy in the future. This article reviews recent advances in the role and mechanism of lncRNAs in tumor radiosensitivity.
Highlights
Among various RNA species, non-coding RNAs are RNA molecules that transcribe but do not encode proteins
This review has summarized the long non-coding RNAs (lncRNAs) that are associated with radiosensitivity via phenomena that include DNA damage repair, apoptosis, CSC regulation, EMT and autophagy
LncRNAs have been demonstrated to be involved in a variety of mechanisms, such as transcriptional regulation, protein modification, translation and formation of RNA-protein or protein-protein complexes
Summary
Jiamin Zhu1,2,*, Shusen Chen2,*, Baixia Yang2,*, Weidong Mao, Xi Yang and Jing Cai. LncRNAs have been found to influence radiosensitivity by regulating various mechanisms, including DNA damage repair, cell cycle arrest, apoptosis, cancer stem cells regulation, epithelial–mesenchymal transition, and autophagy. LncRNAs affect biological pathways in various cancers through different mechanisms and influence the expression of target genes at both the transcriptional and post-transcriptional levels. Sensitivity to radiotherapy is the key to its therapeutic effect on malignant tumors and is a complex process associated with multiple genes, factors, and mechanisms. The effect of radiotherapy is determined by following the 4’Rs of radiobiology: repair of DNA damage, redistribution of the cell cycle, repopulation of tumors, and reoxygenation of hypoxic tumor areas [9]. Previous studies have indicated that lncRNAs influence radioresistance through mechanisms (Table 1 and Figure 1) that include repair of DNA damage, cell cycle arrest, apoptosis, CSCs regulation, epithelial–mesenchymal
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