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Long non-coding RNA CCAT1 acts as an oncogene to promote radiation resistance in lung adenocarcinoma: an epigenomics-based investigation

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Abstract

Long non-coding RNAs (lncRNAs) appear to be the crucial modulators in various processes and critically influence the oncogenesis. As one of the LncRNAs, LncRNA CCAT1 has been reported to be closely associated with the progression multiple cancers, but its role in modulating the radioresistance of lung adenocarcinoma (LUAD) remains unclear. In our present study, we screened the potential radioresistance related LncRNAs in LUAD based on the data from The Cancer Genome Atlas (TCGA) database. Data suggested that CCAT1 was abundantly expressed in LUAD and CCAT1 was significantly associated with poor prognosis and radioresistance. Moreover, our in vitro experiments showed that radiation treatment could trigger elevated expression of CCAT1 in the human LUAD cell lines. Further loss/gain-of-function investigations indicated that CCAT1 knockdown significantly inhibited cell proliferation, migration and promoted cell apoptosis in NCI-H1299 cells under irradiation, whereas CCAT1 overexpression in A549 cells yield the opposite effects. In summary, we identified the promoting role of CCAT1 in radioresistance of LUAD, which may provide a theoretical basis for radiotherapy sensitization of LUAD.

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The data generated in this study are available within the article and its supplementary data files.

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Funding

This research was supported by the Haiyan Fund Project of Harbin Medical University Cancer Hospital (JJZD 2016-06).

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Xiangying Xu conceived and designed this research. Jian Li, Shengnan Guo and Tianhao Li performed the experiments and Songliu Hu, Jianyu Xu conducted the data analysis. Jian Li and Shengnan Guo drafted the manuscript and that was reviewed by Xiangying Xu. All the authors have confirmed the submission of this manuscript.

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Correspondence to Xiangying Xu.

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Li, J., Guo, S., Li, T. et al. Long non-coding RNA CCAT1 acts as an oncogene to promote radiation resistance in lung adenocarcinoma: an epigenomics-based investigation. Funct Integr Genomics 24, 52 (2024). https://doi.org/10.1007/s10142-024-01330-1

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