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Published on: May 24, 2024
Differential expression of long non-coding RNAs during genotoxic stress-induced apoptosis in HeLa and MCF-7 cells
Emre Özgür1, Ufuk Mert, Mustafa Isin
1Department of Basic Oncology, Institute of Oncology, Istanbul University, 34390 Capa, Istanbul, Turkey.
Abstract:
Long non-coding RNAs (lncRNAs) are emerging as new players in cancer as they are implicated in diverse biological processes and aberrantly expressed in a variety of human cancers. No data are available on their function under genotoxic stress-induced apoptosis. In this work, we assessed the behavior of some candidate lncRNAs (HOTAIR, MALAT1, TUG1, lincRNA-p21, GAS5, MEG3, PANDA, UCA1, ANRIL, and CCND1) during DNA damage-induced cell death in HeLa and caspase-3-deficient MCF-7 cells using bleomycin (BLM) and γ-radiation to induce DNA damage. Cells were incubated in the presence of BLM for 24 h or irradiated. Apoptosis was analyzed by measurement of oligonucleosomal fragmentation of nuclear DNA. Our results reveal that basal RNA expression levels as well as the changes in the lncRNA expression rates during genotoxic stress-induced apoptosis were cell-type and/or DNA-damaging agent-specific. Generally, we found that some of the RNA molecules (HOTAIR and MALAT1) are down-regulated while many of them (lincRNA-p21, GAS5, MEG3, ANRIL, and ncRNA-CCND1) are up-regulated and some others (TUG1, UCA1, and PANDA) not affected. The decline in the expression of HOTAIR (approx. twofold, p < 0.01) and MALAT1 (approx 1.6-fold, p < 0.01) was clearly evident in BLM-treated HeLa and MCF cells (only HOTAIR, fivefold, p < 0.01). For lincRNA-p21, ncRNA-CCND1, and MEG3, a similar up-regulation pattern was obvious in both cell lines where the increase was generally more pronounced in BLM-treated cells. Interestingly, the induction of ANRIL and GAS5 was mainly restricted to irradiated cells. In conclusion, our findings reveal a differential regulation of individual lncRNAs during genotoxic stress-induced apoptosis.
Insights
Long non-coding RNAs (lncRNAs) show varied responses to DNA damage-induced apoptosis. Their expression changes are specific to cell type and DNA-damaging agents, impacting cancer research.
Area of Science:
- Molecular Biology
- Cancer Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in biological processes.
- Aberrant lncRNA expression is observed in various human cancers.
- The function of lncRNAs during genotoxic stress-induced apoptosis remains largely unexplored.
Purpose of the Study:
- To investigate the expression patterns of selected lncRNAs under genotoxic stress.
- To determine if lncRNA behavior during DNA damage-induced apoptosis is cell-type or DNA-damaging agent-specific.
Main Methods:
- Assessed expression of ten candidate lncRNAs (HOTAIR, MALAT1, TUG1, lincRNA-p21, GAS5, MEG3, PANDA, UCA1, ANRIL, and CCND1).
- Induced DNA damage using bleomycin (BLM) and gamma radiation in HeLa and MCF-7 cells.
- Analyzed apoptosis via measurement of oligonucleosomal DNA fragmentation.
Main Results:
- Basal and stress-induced lncRNA expression levels were cell-type and DNA-damaging agent-specific.
- HOTAIR and MALAT1 were generally down-regulated, while lincRNA-p21, GAS5, MEG3, ANRIL, and ncRNA-CCND1 were up-regulated.
- TUG1, UCA1, and PANDA showed no significant expression changes; ANRIL and GAS5 induction was specific to irradiated cells.
Conclusions:
- lncRNA regulation during genotoxic stress-induced apoptosis is highly differential.
- These findings provide insights into lncRNA roles in cellular responses to DNA damage.
- Understanding lncRNA dynamics in apoptosis is crucial for cancer research and therapeutic strategies.
