Abstract
The DNA damage response (DDR) is a crucial cellular signaling pathway activated in response to DNA damage, including damage caused by chemotherapy. Chemoresistance, which refers to the resistance of cancer cells to the effects of chemotherapy, poses a significant challenge in cancer treatment. Understanding the relationship between DDR and chemoresistance is vital for devising strategies to overcome this resistance and improve treatment outcomes. Long non-coding RNAs (lncRNAs) are a class of RNA molecules that do not code for proteins but play important roles in various biological processes, including cancer development and chemoresistance. RNA-binding proteins (RBPs) are a group of proteins that bind to RNA molecules and regulate their functions. The interaction between lncRNAs and RBPs has been found to regulate gene expression at the post-transcriptional level, thereby influencing various cellular processes, including DDR signaling pathways. Multiple studies have demonstrated that lncRNAs can interact with RBPs to modulate the expression of genes involved in cancer chemoresistance by impacting DDR signaling pathways. Conversely, RBPs can regulate the expression and function of lncRNAs involved in DDR. Exploring these interactions can provide valuable insights for the development of innovative therapeutic approaches to overcome chemoresistance in cancer patients. This review article aims to summarize recent research on the interaction between lncRNAs and RBPs during cancer chemotherapy, with a specific focus on DDR pathways.
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Abbreviations
- DDR:
-
DNA damage response
- RBPs:
-
RNA-binding proteins
- SSBs:
-
Single-strand breaks
- DSBs:
-
Double-strand breaks
- BER:
-
Base excision repair
- NER:
-
Nucleotide excision repair
- MMR:
-
Mismatch repair
- HR:
-
Homologous recombination
- NHEJ:
-
Nonhomologous end joining
- lncRNAs:
-
Long non-coding RNAs
- MALAT1:
-
Metastasis-associated lung adenocarcinoma transcript 1
- NEAT1:
-
Nuclear-enriched abundant transcript 1
- HGBC:
-
Highly expressed in gallbladder carcinoma
- HOTAIR:
-
HOX antisense intergenic RNA
- RMRP:
-
RNA component of mitochondrial RNA processing endoribonuclease
- TUG1:
-
Taurine upregulated 1
- HULC:
-
Highly up-regulated in liver cancer
- H19:
-
H19 imprinted maternally expressed transcript
- TP53TG1:
-
TP53 target gene 1
- ADAMTS9-AS2:
-
ADAM metallopeptidase with thrombospondin type 1 motif 9 antisense RNA 2
- SNHG12:
-
Small nucleolar RNA host gene 12
- Linc00672:
-
Long intergenic nonprotein-coding RNA
- NSCLC:
-
Non-small cell lung cancer
- CASC2:
-
Cancer susceptibility candidate 2
- CDCA3:
-
Cell division cycle-associated protein 3
- FUS:
-
Fused in sarcoma
- TNBC:
-
Triple-negative breast cancer
- ATM:
-
Ataxia-telangiectasia mutated
- ATR:
-
ATM- and Rad3-related
- CHK1 and CHK2:
-
Cell cycle checkpoint kinases 1 and 2
- IAPs:
-
Inhibitor of apoptosis proteins
- CRC:
-
Colorectal cancer
- DOX:
-
Doxorubicin
- PTX:
-
Paclitaxel
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HSH, FA, YP, and FH: wrote the draft and revised it. HSH and BY: designed and supervised the study. SFT, VV, MM, and MGH: collected the data and designed the figures. All the authors read and approved the submitted version.
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Alemi, F., Poornajaf, Y., Hosseini, F. et al. Interaction between lncRNAs and RNA-binding proteins (RBPs) influences DNA damage response in cancer chemoresistance. Mol Biol Rep 51, 308 (2024). https://doi.org/10.1007/s11033-024-09288-w
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DOI: https://doi.org/10.1007/s11033-024-09288-w