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FGF13 suppresses acute myeloid leukemia by regulating bone marrow niches

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Abstract

Fibroblast growth factor 13 (FGF13) is aberrantly expressed in multiple cancer types, suggesting its essential role in tumorigenesis. Hence, we aimed to explore its definite role in the development of acute myeloid leukemia (AML) and emphasize its associations with bone marrow niches. Results showed that FGF13 was lowly expressed in patients with AML and that its elevated expression was related to prolonged overall survival (OS). Univariate and multivariate Cox regression analyses identified FGF13 as an independent prognostic factor. A prognostic nomogram integrating FGF13 and clinicopathologic variables was constructed to predict 1-, 3-, and 5-year OS. Gene mutation and functional analyses indicated that FGF13 was not associated with AML driver mutations but was related to bone marrow niches. As for immunity, FGF13 was remarkably associated with T cell count, immune checkpoint genes, and cytokines. In addition, FGF13 overexpression substantially inhibited the growth and significantly induced the early apoptosis of AML cells. The xenograft study indicated that FGF13 overexpression prolonged the survival of recipient mice. Overall, FGF13 could serve as an independent prognostic factor for AML, and it was closely related to the bone marrow microenvironment.

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Acknowledgements

This work was supported by the National Key Research and Development Program of China (No. 2019YFA0905900).

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Correspondence to Kai Xue or Junmin Li.

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Ran Li, Kai Xue, and Junmin Li declare no conflict of interest. The study involved animals that were maintained and treated in accordance with Chinese legal requirements. The experiments were approved by the Ethics Committee of Ruijin Hospital Clinical Research Center, Shanghai Jiao Tong University School of Medicine, and the rules were strictly followed during the experiments.

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Li, R., Xue, K. & Li, J. FGF13 suppresses acute myeloid leukemia by regulating bone marrow niches. Front. Med. 16, 896–908 (2022). https://doi.org/10.1007/s11684-022-0944-z

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