Expression of RNA-binding motif 10 is associated with advanced tumor stage and malignant behaviors of lung adenocarcinoma cancer cells

Guan, Guofang; Li, Ranwei; Tang, Wen‐Fang; Liu, Tiecheng; Su, Zheng; Wang, Yan; Jingjin, Tan; Jiang, Shan; Wang, Ke

doi:10.1177/1010428317691740

Cited by 11 publications

(14 citation statements)

References 33 publications

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“…Although RBM10 has been shown to control cancer cell proliferation by differentially regulating NUMB alternative splicing [11] and its expression is associated with advanced tumor stage [12], much more need to learn about its role in cancer development. In attempt to address this question, we first searched genomic and gene expression databases for RBM10 status.…”

Section: Overexpression Of Rbm10 Inhibits Cancer Cell Proliferation Amentioning

confidence: 99%

RNA-binding motif protein 10 induces apoptosis and suppresses proliferation by activating p53

et al. 2019

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RNA-binding motif protein 10 (RBM10) is an RNA-binding protein frequently deleted or mutated in lung cancer cells. Recent reports showed that knockdown of RBM10 in human cancer cells enhances growth of mouse tumor xenografts, suggesting that RBM10 acts as a tumor suppressor. RBM10 also regulates alternative splicing and controls cancer cell proliferation. However, the underlying molecular mechanisms for its tumor suppression role remain largely unclear. Here, we for the first-time report that RBM10 can induce apoptosis and inhibit cancer cell proliferation by activating p53. Our analysis of cancer genomic databases showed that patients with wild type RBM10 and p53 survive longer than do those with mutated p53 or less RBM10. RBM10 overexpression markedly inhibited mitochondrial respiration, cell migration and proliferation of various cancer cells that harbor wild type p53. Also, RBM10 overexpression elongated p53's halflife by disrupting MDM2-p53 interaction and subsequently repressing p53 ubiquitination, whereas knockdown of RBM10 decreased p53 stability. Altogether, our results demonstrate that RBM10 inhibits cancer cell proliferation and induces apoptosis in part by blocking the MDM2-p53 feedback loop.

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Section: Overexpression Of Rbm10 Inhibits Cancer Cell Proliferation Amentioning

confidence: 99%

RNA-binding motif protein 10 induces apoptosis and suppresses proliferation by activating p53

et al. 2019

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“…There is substantial evidence pointing to the pro-survival and anti-apoptotic roles of BIRC3 in cancer cells; however, not all data are consistent ( Frazzi, 2021 ). An in vitro study showed that RNA-binding motif 10 overexpression inhibited the malignant behaviors of A549 and H1299 cells by inducing the expression of AKT2, BIRC3, and JUN ( Guan et al, 2017 ). However, Dubois et al (2019) reported that overexpression of BIRC3 regulated by RASSF1A depletion decreased the rate of cancer cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Analysis of Inhibitor of Apoptosis Protein Expression and Prognostic Significance in Non–Small Cell Lung Cancer

Lee

Huang

et al. 2021

Front. Genet.

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Inhibitors of apoptosis proteins (IAPs) have been associated with tumor development and progression by affecting apoptosis through cell death signaling pathways. To date, eight IAPs (BIRC1–8) have been identified in mammalian cells. However, the role of IAPs in non–small cell lung cancer (NSCLC) development and progression has not been explored in depth. In this study, we used public datasets and bioinformatics tools to compare the expression, prognostic significance, and function of IAPs in NSCLC and its subtypes. Expression of IAPs in cancer and normal tissues and at different stages of NSCLC was compared with gene expression profiling interactive analysis, and their prognostic significance was analyzed with the Kaplan–Meier Plotter database. The correlations among IAPs were analyzed with the STRING database and SPSS19.0. Functional annotation of IAPs was analyzed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment on the basis of the DAVID tool. Among patients with lung adenocarcinoma (LUAD), the expression level of BIRC5 was higher than that in normal samples, and the expression of BIRC1 and BIRC5 significantly varied in different stages. Moreover, the BIRC1–3 and BIRC5 mRNA levels were associated with overall survival (OS), and the BIRC1–2 and BIRC5–6 mRNA levels were associated with progression-free survival (PFS). Among patients with lung squamous cell carcinoma (LUSC), the expression level of BIRC1 was lower and that of BIRC5 was higher than those in normal tissues, and BIRC5 expression significantly varied in different stages. BIRC1 expression was associated with OS, whereas BIRC2 and BIRC6 expression was associated with PFS. Enrichment analysis showed that most IAPs are associated with ubiquitin- and apoptosis-related pathways. Collectively, this study suggests BIRC5 as a potential diagnostic and staging marker, BIRC1 as a potential marker of OS, and BIRC2 and BIRC6 as potential PFS markers for patients with NSCLC. These highlight new targets for the early detection, treatment, and management of NSCLC.

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“…A total of 690 genes that were regulated by RBM10 expression in A549 cells were identified, of which 304 were up‐regulated and 386 were down‐regulated. Among these, RAP1A expression was the most down‐regulated (63.5%); thus, we explored its downstream signalling pathway. RAP1A is a type of Ras‐associated protein 1 (RAP1), with 95% sequence homology to RAP1B .…”

Section: Introductionmentioning

confidence: 99%

“…In this study, we aimed to explore the effect of RBM10 overexpression and knockdown on the proliferation of lung adenocarcinoma cells as well as the affected downstream pathways by assessing the expression of several regulatory proteins that have previously been identified as being modulated by RBM10 . We then sought to verify the effect of RBM10 overexpression and inhibition in vivo in BALB/c mice.…”

Section: Introductionmentioning

confidence: 99%

RBM10 inhibits cell proliferation of lung adenocarcinoma via RAP1/AKT/CREB signalling pathway

Jin

Wang

et al. 2019

J Cellular Molecular Medi

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Initial functional studies have demonstrated that RNA‐binding motif protein 10 (RBM10) can promote apoptosis and suppress cell proliferation; however, the results of several studies suggest a tumour‐promoting role for RBM10. Herein, we assessed the involvement of RBM10 in lung adenocarcinoma cell proliferation and explored the potential molecular mechanism. We found that, both in vitro and in vivo, RBM10 overexpression suppresses lung adenocarcinoma cell proliferation, while its knockdown enhances cell proliferation. Using complementary DNA microarray analysis, we previously found that RBM10 overexpression induces significant down‐regulation of RAP1A expression. In this study, we have confirmed that RBM10 decreases the activation of RAP1 and found that EPAC stimulation and inhibition can abolish the effects of RBM10 knockdown and overexpression, respectively, and regulate cell growth. This effect of RBM10 on proliferation was independent of the MAPK/ERK and P38/MAPK signalling pathways. We found that RBM10 reduces the phosphorylation of CREB via the AKT signalling pathway, suggesting that RBM10 exhibits its effect on lung adenocarcinoma cell proliferation via the RAP1/AKT/CREB signalling pathway.

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Expression of RNA-binding motif 10 is associated with advanced tumor stage and malignant behaviors of lung adenocarcinoma cancer cells

Cited by 11 publications

References 33 publications

RNA-binding motif protein 10 induces apoptosis and suppresses proliferation by activating p53

RNA-binding motif protein 10 induces apoptosis and suppresses proliferation by activating p53

Comprehensive Analysis of Inhibitor of Apoptosis Protein Expression and Prognostic Significance in Non–Small Cell Lung Cancer

RBM10 inhibits cell proliferation of lung adenocarcinoma via RAP1/AKT/CREB signalling pathway

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