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RBM38 in cancer: role and mechanism

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Abstract

Cancer is the second leading cause of death globally. Abnormity in gene expression regulation characterizes the trajectory of tumor development and progression. RNA-binding proteins (RBPs) are widely dysregulated, and thus implicated, in numerous human cancers. RBPs mainly regulate gene expression post-transcriptionally, but emerging studies suggest that many RBPs can impact transcription by acting on chromatin as transcription factors (TFs) or cofactors. Here, we review the evidence that RBM38, an intensively studied RBP, frequently plays a tumor-suppressive role in multiple human cancer types. Genetic studies in mice deficient in RBM38 on different p53 status also establish RBM38 as a tumor suppressor (TS). By uncovering a spectrum of transcripts bound by RBM38, we discuss the diversity in its mechanisms of action in distinct biological contexts. Examination of the genomic features and expression pattern of RBM38 in human tissues reveals that it is generally lost but rarely mutated, in cancers. By assessing future trends in the study of RBM38 in cancer, we signify the possibility of targeting RBM38 and its related pathways as therapeutic strategies against cancer.

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Acknowledgements

This project was supported by Grants from the National Natural Science Foundation of China 81972418 (to D. Z.) and 31871481 (to Z. D.), the Wuhan Frontier Science and Technology Program 2019020701011490 (to D. Z.) and the Fundamental Research Funds for the Central Universities 531119200130 (to D. Z.) and 2662017PY109 (to Z. D).

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Zou, C., Wan, Y., He, L. et al. RBM38 in cancer: role and mechanism. Cell. Mol. Life Sci. 78, 117–128 (2021). https://doi.org/10.1007/s00018-020-03593-w

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