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C-Fos-activated circRPPH1 contributes to glioma stemness

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Abstract

Objective

Cancer stem cells or cancer stemness has been confirmed to a major obstacle for glioma progression and it has also been reported that circRNAs play an important part in cancer progression. This study mainly focuses on revealing the role of circRPPH1 and the underlying mechanisms in glioma cell stemness.

Methods

In vitro experiment including RT-qPCR, Western blot, sphere-formation analysis, and ALDH1 activity, and in vivo tumorigenesis experiments were performed to evaluate the effects of circRPPH1 on glioma cell stemness. Luciferase reporter, ChIP, and DNA pull-down analysis were used to reveal the underlying mechanisms.

Results

It was found that circRPPH1 level was upregulated in glioma cell spheres and facilitated the stemness of glioma cells; C-FOS transcriptionally activated circRPPH1 expression via directly binding to circRPPH1 promoter in glioma cells. Moreover, circRPPH1 promoted the stemness of glioma cells dependent on c-FOS-mediated transcriptional activation.

Conclusions

This study indicates that c-Fos-activated circRPPH1 contributes to glioma stemness and provides a potential target for glioma progression based on the c-FOS/circRPPH1 regulatory axis.

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Data availability statement

All data generated or analyzed during this study are included in this published article.

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Acknowledgements

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Authors and Affiliations

Authors

Contributions

GX designed the research. GX, JQ, MZ, and QW performed the research. GX and JQ wrote the manuscript. MZ re-reviewed the manuscript.

Corresponding author

Correspondence to Gang Xu.

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The authors declare no conflict of interest.

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All the experiments were obtained the approval of the Ethics Committee for Animal Experimentation of the Second Affiliated Hospital of Xi'an Jiaotong University.

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Xu, G., Qu, J., Zhang, M. et al. C-Fos-activated circRPPH1 contributes to glioma stemness. Clin Transl Oncol 25, 1277–1286 (2023). https://doi.org/10.1007/s12094-022-03022-3

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  • DOI: https://doi.org/10.1007/s12094-022-03022-3

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