The expression of RNA-binding protein RBM38 decreased in renal cell carcinoma and represses renal cancer cell proliferation, migration, and invasion

Huang, Wen; Wei, Xiaolong; Ni, Wei‐Wei; Cao, Mengda; Meng, Ling; Yang, Haiwei

doi:10.1177/1010428317701635

Cited by 20 publications

(22 citation statements)

References 36 publications

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“…Recently, we have identified a potential tumor suppressor RBM38 (as known as RNPC1) in breast cancer [ 19 ], which also exhibited a tumor suppressor functions in colorectal cancer [ 20 ], acute myeloid leukemia [ 21 ], renal cell carcinoma [ 22 ] and hepatocellular carcinoma [ 23 ]. As a target of p53 and a member of RNA-binding protein (RBP), RBM38 played a significant role in post-transcriptional regulation, mRNA splicing, surveillance, stabilization and translation in gene expression [ 19 , 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

PTEN expression is upregulated by a RNA-binding protein RBM38 via enhancing its mRNA stability in breast cancer

Zhou

Shi

et al. 2017

J Exp Clin Cancer Res

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BackgroundPTEN (phosphatase and tensin homolog gene on chromosome 10), a well-characterized tumor suppressor, is a key regulator of the phosphatidylinositol-3-kinase (PI3K)/AKT pathway involved in cell survival, metastasis and cell renewal. PTEN expression is closely related to the phenotype, prognosis and drug selection in breast cancer. It is mainly regulated by transcriptional and post-transcriptional modifications. RNA binding motif protein 38 (RBM38), an RNA-binding protein (RBP) and a target of P53 family, plays a crucial role in the regulation of cellular processing, especially in post-transcription regulation and gene transcription. In this study, we investigated a new post-transcription regulation mechanism of PTEN expression by RBM38 in breast cancer.MethodsImmunohistochemistry, lentivirus transfections, Western blotting analysis, qRT-PCR and ELISA were used to conduct the relation between RBM38 and PTEN. RNA immunoprecipitation, RNA electrophoretic mobility shift and dual-luciferase reporter assays were employed to identify the direct binding sites of RBM38 with PTEN transcript. Colony formation assay was conducted to confirm the function of PTEN in RBM38-induced growth suppression.ResultsPTEN expression was positively associated with the expression of RBM38 in breast cancer tissues and breast cancer cells. Moreover, RBM38 stabilized PTEN transcript to enhance PTEN expression via binding to multiple AU/U- rich elements (AREs) in 3′-untranslated region (3′-UTR) of PTEN transcript. Additionally, specific inhibitors of PTEN activity and small interfering (siRNA) of PTEN expression inhibited RBM38-mediated suppression of proliferation, which implied that RBM38 acted as a tumor suppressor partly by enhancing PTEN expression.ConclusionThe present study revealed a new PTEN regulating mechanism that PTEN was positively regulated by RBM38 via stabilizing its transcript stability, which in turn alleviated RBM38-mediated growth suppression.Electronic supplementary materialThe online version of this article (10.1186/s13046-017-0620-3) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

PTEN expression is upregulated by a RNA-binding protein RBM38 via enhancing its mRNA stability in breast cancer

Zhou

Shi

et al. 2017

J Exp Clin Cancer Res

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“…In ccRCC, many RBPs have been revealed playing important roles in tumorigenesis [7,24]. RBPs have different functions, where some RBPs can enhance tumorigenesis [10,11], and some RBPs can repress tumorigenesis [8,9,12]. Taking into account the important roles of RBPs in ccRCC, we comprehensively explored the roles of all these RBPs in ccRCC using consensus clustering method.…”

Section: Discussionmentioning

confidence: 99%

“…CIPP is up-regulated in ccRCC and CIPP de ciency can inhibit proliferation and enhance the chemosensitivity to gemcitabine in ccRCC [11]. RBM38 acts as a tumor suppressor in ccRCC, which can inhibit tumor proliferation, migration and invasion through in uencing their target RNA stability [12]. However, most of the RBPs that involved in tumorigenesis and progression of ccRCC remain undetermined.…”

Section: Introductionmentioning

confidence: 99%

Integrated analysis of the functions of RNA binding proteins in clear cell renal cell carcinoma

Hua¹,

Chen

Ge³

et al. 2021

Genomics

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Background: RNA binding proteins (RBPs) dysregulation is involved in the process es of various tumor. However, the roles of RBPs in clear cell renal cell carcinoma (ccRCC) remain poorly understand. Systematic exploration of the roles of RBPs in ccRCC may provide new insights for the treatments of ccRCC. Methods: Expression data of RBPs was obtained from The Cancer Genome Atlas database. The roles of RBPs in ccRCC were systematically investigated using consensus clustering methods. Differentially expressed RBPs between normal and tumor tissues were obtained. Protein-protein interaction (PPI) network was constructed using "STRING" software. The expression levels of hub genes were validated in The Human Protein Atlas (HPA) database and receiver operating characteristic (ROC) curves were used to evaluate diagnostic value. Univariate and Lasso Cox regression and Kaplan-Meier curves were used to screen the most useful prognostic genes. Multivariate Cox regression was performed to construct a risk score model. The e ciency of the model was evaluated using time-dependent ROC and Kaplan-Meier curves, and validated in E-MTAB-3267 set. Results: Two clusters were identi ed based on the expression similarity of RBPs, and the cluster 2 was closely correlated with the malignancy of ccRCC. Several oncogenic pathways, including epithelial mesenchymal transition, G2M checkpoint, KRAS signaling and IL6 JAK STAT3 signaling were enriched in cluster 2. In addition, we obtained 115 differently expressed RBPs in ccRCC, comprising 71 up-regulated and 44 down-regulated ones. Ten hub RBPs with good diagnostic value were obtained from PPI network and validated in HPA database. Ten RBPs were identi ed as survival-related genes and used to construct a risk score model. The model could be used to stratify patients with different prognosis. We found highrisk patients tended to be advanced stage, high grade, high pathological T staging and could be an independent risk factor for overall survival of ccRCC patients. Conclusions: We identi ed ten RBPs with diagnostic value, which might be the potential diagnostic biomarkers for ccRCC. A risk score model was established to stratify patients and could be used as a complementation for clinical factors to guide clinical practice in the future.

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“…In cancer cells Rbm38 fulfils different functions: originally it was described to be an oncogene in gastrointestinal system and malignant lymphomas as well as in breast and prostate cancer 12 , 27 , 28 . Recent studies suggest that Rbm38 can also operate as a tumour suppressor 9 , 10 , 29 . Rbm38 is known to be expressed in hematopoietic organs (bone marrow, spleen and thymus).…”

Section: Discussionmentioning

confidence: 99%

Therapeutic modulation of RNA-binding protein Rbm38 facilitates re-endothelialization after arterial injury

Sonnenschein

Fiedler

Pfanne

et al. 2019

Cardiovascular Research

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Aims Delayed re-endothelialization after balloon angioplasty in patients with coronary or peripheral artery disease impairs vascular healing and leads to neointimal proliferation. In the present study, we examined the effect of RNA-binding motif protein 38 (Rbm38) during re-endothelialization in a murine model of experimental vascular injury. Methods and results Left common carotid arteries of C57BL/6 mice were electrically denudated and endothelial regeneration was evaluated. Profiling of RNA-binding proteins revealed dysregulated expression of Rbm38 in the denudated and regenerated areas. We next tested the importance of Rbm38 in human umbilical vein endothelial cells (HUVECS) and analysed its effects on cellular proliferation, migration and apoptosis. Rbm38 silencing in vitro demonstrated important beneficial functional effects on migratory capacity and proliferation of endothelial cells. In vivo, local silencing of Rbm38 also improved re-endothelialization of denuded carotid arteries. Luciferase reporter assay identified miR-98 and let-7f to regulate Rbm38 and the positive proliferative properties of Rbm38 silencing in vitro and in vivo were mimicked by therapeutic overexpression of these miRNAs. Conclusion The present data identified Rbm38 as an important factor of the regulation of various endothelial cell functions. Local inhibition of Rbm38 as well as overexpression of the upstream regulators miR-98 and let-7f improved endothelial regeneration in vivo and thus may be a novel therapeutic entry point to avoid endothelial damage after balloon angioplasty.

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The expression of RNA-binding protein RBM38 decreased in renal cell carcinoma and represses renal cancer cell proliferation, migration, and invasion

Cited by 20 publications

References 36 publications

PTEN expression is upregulated by a RNA-binding protein RBM38 via enhancing its mRNA stability in breast cancer

PTEN expression is upregulated by a RNA-binding protein RBM38 via enhancing its mRNA stability in breast cancer

Integrated analysis of the functions of RNA binding proteins in clear cell renal cell carcinoma

Therapeutic modulation of RNA-binding protein Rbm38 facilitates re-endothelialization after arterial injury

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