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RBM24 Suppresses the Tumorigenesis of Glioblastoma by Stabilizing LATS1 mRNA

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Abstract

The ribose nucleic acid (RNA)-binding motif protein 24 (RBM24) has been recognized as a critical regulatory protein in various types of tumors. However, its specific role in glioblastoma (GBM) has not been thoroughly investigated. The objective of this study is to uncover the role of RBM24 in GBM and understand the underlying mechanism. The expression of RBM24 in GBM was initially analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA). Subsequently, the RBM24 expression levels in clinical samples of GBM were examined, and the survival curves of GBM patients were plotted based on high- and low-expression levels of RBM24 using Kaplan–Meier (KM) plotter. In addition, RBM24 knockdown cell lines and overexpression vectors were created to assess the effects on proliferation, apoptosis, and invasion abilities. Finally, the binding level of RBM24 protein to LATS1 messenger RNA (mRNA) was determined by RNA immunoprecipitation (RIP) assay, and the expression levels of RBM24 and LATS1 were measured through quantitative reverse-transcriptase-polymerase chain reaction (qRT-PCR) and Western blot (WB). Our data revealed a significant decrease in RBM24 mRNA and protein levels in GBM patients, indicating that those with low RBM24 expression had a worse prognosis. Overexpression of RBM24 led to inhibited cell proliferation, reduced invasion, and increased apoptosis in LN229 and U87 cells. In addition, knocking down LATS1 partially reversed the effects of RBM24 on cell proliferation, invasion, and apoptosis in GBM cells. In vivo xenograft model further demonstrated that RBM24 overexpression reduced the growth of subcutaneous tumors in nude mice, accompanied by a decrease in Ki-67 expression and an increase in apoptotic events in tumor tissues. There was also correlation between RBM24 and LATS1 protein expression in the xenograft tumors. RBM24 functions to stabilize LATS1 mRNA, thereby inhibiting the proliferation, suppressing invasion, and promoting apoptosis in GBM cells.

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Data Availability

The datasets used and/or analyzed during the current study are available from the corresponding author via email request.

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The authors received no financial support for the research authorship and/or publication of this article.

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Hao Ye and Xuewen Lu mainly participated in literature search, study design, writing and critical revision, prepared Figs. 1, 2, and 3. Xuewen Lu, Yong Xie, Guolin Ding and Wei Sun mainly participated in data collection, data analysis and data interpretation, prepared Figs. 4 and 5. All authors read and approved the final manuscript.

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Correspondence to Hao Ye.

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The study was approved by the Ethical Committee of the First People’s Hospital of Qujing. Patients provided a signed informed consent form for the sample collection. The protocols for all animal studies were observed and approved by the Animal Care and Use Committee of the First People’s Hospital of Qujing.

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Lu, X., Xie, Y., Ding, G. et al. RBM24 Suppresses the Tumorigenesis of Glioblastoma by Stabilizing LATS1 mRNA. Biochem Genet (2024). https://doi.org/10.1007/s10528-024-10715-7

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