Abstract

The RNA-binding motif protein 10 (RBM10) is involved in alternative splicing and modifies mRNA post-transcriptionally. RBM10 is abnormally expressed in the lung, breast, and colorectal cancer, female genital tumors, osteosarcoma, and other malignant tumors. It can inhibit proliferation, promote apoptosis, and inhibit invasion and metastasis. RBM10 has long been considered a tumor suppressor because it promotes apoptosis through the regulation of the MDM2-p53 negative feedback loop, Bcl-2, Bax, and other apoptotic proteins and inhibits proliferation through the Notch signaling and rap1a/Akt/CREB pathways. However, it has been recently demonstrated that RBM10 can also promote cancer. Given these different views, it is necessary to summarize the research progress of RBM10 in various fields to reasonably analyze the underlying molecular mechanisms, and provide new ideas and directions for the clinical research of RBM10 in various cancer types. In this review, we provide a new perspective on the reasons for these opposing effects on cancer biology, molecular mechanisms, research progress, and clinical value of RBM10.

Highlights

  • The occurrence of cancer is the result of the imbalance of intracellular homeostasis and its multiple regulatory mechanisms

  • Previous RNA-binding motif protein 10 (RBM10) research mainly focused on apoptosis and proliferation pathway; more and more studies show that it plays an important role in metastasis and invasion

  • These results suggest that RBM10 mediated cell proliferation is not dependent on MAPK/ERK and p38 MAPK signaling pathways

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Summary

INTRODUCTION

The occurrence of cancer is the result of the imbalance of intracellular homeostasis and its multiple regulatory mechanisms. RNA-binding motif protein 10 (RBM10), one of the most important members of the RBP family, is an alternative RNA splicing factor that participates in the regulation of gene expression. RBM10 has high sequence homology with RBM5 at the amino acid level, and both play an important role in the regulation of apoptosis [10]. The preference order of RBM5 for RNA is poly G > poly C > poly A> poly U [14] These preferences show that RBM proteins have different target genes and play different roles in alternative splicing. RBM10v1 and RBM10v2 share 60– 64% homology with RBM5 when exons 4, 9 and 15 are excluded, indicating that the remaining amino acid sequences are highly conserved among the three proteins. Exons 9 and 15 are shared by the two RBM10 variants, but are different from those of RBM5, suggesting these sequences may influence the different functions of RBM10 and RBM5 (Figure 1) [17]

ALTERNATIVE SPLICING
Invasion and Metastasis
Tumorigenesis chromosome division
Findings
AUTHOR CONTRIBUTIONS
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