RBM38 is involved in TGF-β-induced epithelial-to-mesenchymal transition by stabilising zonula occludens-1 mRNA in breast cancer

Wu, Jing; Zhou, Xu‐Jie; Sun, Xi; Xia, Tiansong; Li, Xiaoxia; Shi, Liang; Zhu, Lei; Zhou, Wenbin; Wei, Ji‐Fu; Ding, Qiang

doi:10.1038/bjc.2017.204

Cited by 39 publications

(36 citation statements)

References 54 publications

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“…Adding to this, disrupted expression level of RBM38 in breast cancer due to the silencing E-box element promoter region by SNAIL [91], propose the indirect effect of HOTAIR on regulation of this tumour suppressor gene. Inhibition of RBM38 activity could destabilize zonula occludens-1, consequently leading to induction of EMT and metastasis [91]. Curiously, evidences emphasize the crucial role of HOTAIR overexpression in breast cancer radioresistance through EMT induction.…”

Section: Epithelial Mesenchymal Transition and Hotairmentioning

confidence: 92%

“…Previous study on hepatocellular malignancy highlighted the remarkable effect of HOTAIR on the blockage of RNA binding motif protein 38 (RBM38), as a tumour suppressor gene [90]. Adding to this, disrupted expression level of RBM38 in breast cancer due to the silencing E-box element promoter region by SNAIL [91], propose the indirect effect of HOTAIR on regulation of this tumour suppressor gene. Inhibition of RBM38 activity could destabilize zonula occludens-1, consequently leading to induction of EMT and metastasis [91].…”

Section: Epithelial Mesenchymal Transition and Hotairmentioning

confidence: 99%

“…Additionally, up-regulation of HOTAIR has been suggested to induce radioresistance in HeLa and C33A cells, in a competition, by prohibiting p21 activity, while up-regulation of p21 could neutralize the negative effect of HOTAIR activity on cell resistance against ionizing radiation [100]. In breast cancer cells, studies demonstrated relation of HOTAIR expression level with metastasis free survival and enhancing rim fraction (ERF) radiogenomics score [91,101]. It can also contribute to radioresistance by function as ceRNA.…”

Section: Hotair and Radiotherapymentioning

confidence: 99%

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The emerging role of the long non-coding RNA HOTAIR in breast cancer development and treatment

2020

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Despite considering vast majority of the transcribed molecules as merely noise RNA in the last decades, recent advances in the field of molecular biology revealed the mysterious role of long non-coding RNAs (lncRNAs), as a massive part of functional non-protein-coding RNAs. As a crucial lncRNA, HOX antisense intergenic RNA (HOTAIR) has been shown to participate in different processes of normal cell development. Aberrant overexpression of this lncRNA contributes to breast cancer progression, through different molecular mechanisms. In this review, we briefly discuss the structure of HOTAIR in the context of genome and impact of this lncRNA on normal human development. We subsequently summarize the potential role of HOTAIR overexpression on different processes of breast cancer development. Ultimately, the relationship of this lncRNA with different therapeutic approaches is discussed.

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Section: Epithelial Mesenchymal Transition and Hotairmentioning

confidence: 92%

Section: Epithelial Mesenchymal Transition and Hotairmentioning

confidence: 99%

Section: Hotair and Radiotherapymentioning

confidence: 99%

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The emerging role of the long non-coding RNA HOTAIR in breast cancer development and treatment

2020

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“…For example, the oncogene crabp2 interacts with the RBP HuR to promote metastasis of lung cancer cells by regulating integrin β1/FAK/ERK signaling (Wu et al, 2019). Transforming growth factor-β (TGF-β) induces the expression of RNA-binding motif protein 38 (RBM38) in breast cancer, which promotes epithelial-to-mesenchymal transition by regulating the zonula occludens-1 transcript (Wu et al, 2017). The forkhead box K2 protein (FOXK2) promotes colorectal cancer metastasis by upregulating mRNA expression of zinc finger E-box binding homeobox 1 (ZEB1) (Du et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Integrated Analysis of the Functions and Prognostic Values of RNA Binding Proteins in Lung Squamous Cell Carcinoma

Xue

Gao

et al. 2020

Front. Genet.

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Lung cancer is the leading cause of cancer-related deaths worldwide. Dysregulation of RNA binding proteins (RBPs) has been found in a variety of cancers and is related to oncogenesis and progression. However, the functions of RBPs in lung squamous cell carcinoma (LUSC) remain unclear. In this study, we obtained gene expression data and corresponding clinical information for LUSC from The Cancer Genome Atlas (TCGA) database, identified aberrantly expressed RBPs between tumors and normal tissue, and conducted a series of bioinformatics analyses to explore the expression and prognostic value of these RBPs. A total of 300 aberrantly expressed RBPs were obtained, comprising 59 downregulated and 241 upregulated RBPs. Functional enrichment analysis indicated that the differentially expressed RBPs were mainly associated with mRNA metabolic processes, RNA processing, RNA modification, regulation of translation, the TGF-beta signaling pathway, and the Toll-like receptor signaling pathway. Nine RBP genes (A1CF, EIF2B5, LSM1, LSM7, MBNL2, RSRC1, TRMU, TTF2, and ZCCHC5) were identified as prognosis-associated hub genes by univariate, least absolute shrinkage and selection operator (LASSO), Kaplan-Meier survival, and multivariate Cox regression analyses, and were used to construct the prognostic model. Further analysis demonstrated that high risk scores for patients were significantly related to poor overall survival according to the model. The area under the time-dependent receiver operator characteristic curve of the prognostic model was 0.712 at 3 years and 0.696 at 5 years. We also developed a nomogram based on nine RBP genes, with internal validation in the TCGA cohort, which showed a favorable predictive efficacy for prognosis in LUSC. Our results provide novel insights into the pathogenesis of LUSC. The nine-RBP gene signature showed predictive value for LUSC prognosis, with potential applications in clinical decision-making and individualized treatment.

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“…It inhibited the proliferation of breast cancer by upregulating the expression of PTEN and down regulating the expression of c-Myc [ 11 , 12 ]. It also increased the stability of ZO-1 (Zonula occludens-1) and inhibited the breast cancer epithelial-mesenchymal transition [ 10 , 13 ]. RBMS3 was also identified to be a potential treatment target in breast cancer which inhibited the proliferation and invasion of breast cancer [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

RBMS2 inhibits the proliferation by stabilizing P21 mRNA in breast cancer

Sun

et al. 2018

J Exp Clin Cancer Res

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BackgroundRNA binding proteins (RBPs) play an important role in regulating the metabolism of target RNAs. Aberrant expression of RBPs plays a vital role in the initiation and development of many cancers. The RBM family, which has the conserved RNA binding motif RNP1 and RNP2, shares the similar function in RNA processing and RBMS2 is a member of them. P21, also named CDKN1A, promotes cell cycle arrest and plays an important role in halting cell proliferation. In our study, we identified RBMS2 as a tumor suppressor in breast cancer. It inhibited the proliferation of breast cancer by positively regulating the stability of P21 mRNA in posttranscriptional way.MethodsTCGA was used to identify differentially expressed RBPs in breast cancer.The effect of RBMS2 on breast cancer proliferation was evaluated in vitro using CCK-8 assays, colony formation assays and cell-cycle assays and the in vivo effect was investigated using a mouse tumorigenicity model.The main pathway and genes regulated by RBMS2 was detected by RNA sequencing. The RNA immunoprecipitation combined with dual-luciferase reporter assay were conducted to testify the direct binding between RBMS2 and P21. Rescue assay was used to detect P21 as the main target of RBMS2.ResultsThe expression of RBMS2 was lower in breast cancer compared with normal tissues and was a favorable biomarker in breast cancer. RBMS2 inhibited the proliferation of breast cancer and P21 was the main target of RBMS2. RBMS2 stabilized the mRNA of P21 by directly binding to the AU-rich element of 3′-UTR region. Anti-proliferation activity induced by overexpression of RBMS2 was rescued by interfering with the expression of P21.ConclusionIn conclusion, RBMS2 acted as a tumor suppressor in breast cancer and positively regulated the expression of P21 by stabilizing its mRNA.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0968-z) contains supplementary material, which is available to authorized users.

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RBM38 is involved in TGF-β-induced epithelial-to-mesenchymal transition by stabilising zonula occludens-1 mRNA in breast cancer

Cited by 39 publications

References 54 publications

The emerging role of the long non-coding RNA HOTAIR in breast cancer development and treatment

The emerging role of the long non-coding RNA HOTAIR in breast cancer development and treatment

Integrated Analysis of the Functions and Prognostic Values of RNA Binding Proteins in Lung Squamous Cell Carcinoma

RBMS2 inhibits the proliferation by stabilizing P21 mRNA in breast cancer

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