RBMS2 inhibits the proliferation by stabilizing P21 mRNA in breast cancer

Sun, Xi; Hu, Yue; Wu, Jing; Shi, Liang; Zhu, Lei; Xi, Pei-Wen; Wei, Ji‐Fu; Ding, Qiang

doi:10.1186/s13046-018-0968-z

Cited by 40 publications

(41 citation statements)

References 33 publications

(35 reference statements)

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“…Furthermore, silencing HOXA-AS2 signi cantly downregulated the expression of EZH2 and upregulated the expression of P21. As an important regulatory factor of cell cycle, P21 protein is closely related to many kinds of cancer occurrence and development (24,25). We speculate that HOXA-AS2 may affect the tumor growth by regulating the expression of EZH2, but the speci c mechanism of HOXA-AS2 in OSSC remains to be studied further.…”

Section: Discussionmentioning

confidence: 89%

Knowdown of lncRNA HOXA-AS2 inhibits proliferation, invasion and migration of oral squamous cell carcinoma

Zhao

Xing

Zhi-gang

et al. 2020

Preprint

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Background Oral squamous cell carcinoma (OSSC) is one of the most common cancers in the world. The aim to the study was to evaluated the biological function and partly underlying regulatory mechanism of lncRNA homeobox A cluster antisense RNA2 (HOXA-AS2) on oral squamous cell carcinoma. Methods The expression of HOXA-AS2 in OSSC cells was detected by quantitative real time polymerase chain reaction (qRT-PCR). HOXA-AS2 expression was modified by transfection with HOXA-AS2 knockdown into TCA-8113 cells. The biological activity of TCA-8113 cells were detected by Cell Counting Kit-8 (CCK-8), EdU staining, Tunel staining, flow cytometry, wound healing, transwell assasy and western blot. The relationship between HOXA-AS2 and EZH2 was analyzed by RNA immunoprecipitation (RIP). Results At first, in this study, HOXA-AS2 expression in TCA-8113 cell line was increased compared with normal oral cells. Furthermore, HOXA-AS2 knockdown could inhibit cell viability, migration and invasion. Besides, EZH2 is the target of HOXA-AS2 in TCA-8113 cells. EZH2 expression was reduced by the HOXA-AS2 knockdown and the expression of P21 was negatively correlated to the expression of HOXA-AS2 in TCA-8113 cells. Conclusion In this study, silencing HOXA-AS2 reduced cell viability, invasion and migration capacity and EZH2, as an oncogene, could be downregulated by HOXA-AS2 knockdown in OSSC cells.

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Section: Discussionmentioning

confidence: 89%

Knowdown of lncRNA HOXA-AS2 inhibits proliferation, invasion and migration of oral squamous cell carcinoma

Zhao

Xing

Zhi-gang

et al. 2020

Preprint

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“…All these results strongly supported that RBM7 acted as an oncogenic role in breast cancer. It was previously found that two other RBMs, RBM38 and RBMS2 acted as tumor suppressor in breast cancers 19 , 22 . Yang et al also found RBMS3 could inhibit breast cancer proliferation and metastasis 31 , 32 .…”

Section: Discussionmentioning

confidence: 99%

“…It was also linked with breast cancer epithelial-to-mesenchymal transition induced by TGF-β via stabilizing zonula occludens-1 mRNA 19 . We also identified another RBP, RBMS2, to stabilize the mRNA of P21 in breast cancer and thereby enhance its regulation 22 . However, the role of RBM7 in cancers, especially in breast cancer, is still unknown.…”

Section: Introductionmentioning

confidence: 86%

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Oncogenic action of the exosome cofactor RBM7 by stabilization of CDK1 mRNA in breast cancer

Zhang

Zhu

et al. 2020

npj Breast Cancer

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RNA exosome can target the specific RNAs for their processing/degradation by distinct exosome cofactors. As a key component in exosome cofactors, RNA binding motif protein 7 (RBM7) shows the binding specificity for uridine-rich sequences in mRNAs via its RNA recognition motifs. However, the specific function of RBM7 in human breast cancer remains unclear. In vitro, experiments revealed that knockdown of RBM7 dramatically inhibited breast cancer cell proliferation, while inducing G1 cell cycle arrest; the opposite was true when RBM7 was overexpressed. Meanwhile, experiments in vivo confirmed the oncogenic function of RBM7 in breast cancer. RNA sequencing and the following pathway analysis found that cyclin-dependent kinase1 (CDK1) was one of the main gene regulated by RBM7. Overexpression of RBM7 increased CDK1 expression, while RBM7 knockdown decreased it. RIP assays additionally found that RBM7 bound directly to CDK1 mRNA. It was also showed that RBM7 could directly bind to the AU-rich elements (AREs) in 3′-UTR of CDK1 mRNA, which contributed to the stability of CDK1 mRNA by lengthening its half-life. More importantly, the oncogenic activity reduced by knockdown of RBM7 could be rescued by overexpression of CDK1 both in vitro and in vivo, but mutant CDK1 failed. All the evidences implied RBM7 promoted breast cancer cell proliferation by stabilizing CDK1 mRNA via binding to AREs in its 3′-UTR. As we knew, it was the first attempt to connect the RNA exosome to the tumor development, providing new insights into the mechanisms of RNA exosome-linked diseases.

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“…P21, also known as CDKN1A which resided in 6p21.2 20,21 , has been investigated involvement in cell cycle regulation, differentiation, cell migration, cytoskeletal dynamic, apoptosis, transcription, DNA repair, induction of totipotent stem cells, autophagy and senescence 22,23 . Commonly accepted is that P21 as a member of cyclin-dependent kinase inhibitors (CDKI) interacts with various cell cycle proteins to mediate G1/S growth phase arrest in response to different stimuli 24,25 .…”

Section: Discussionmentioning

confidence: 99%

KRT23 Acts as an Oncogene in Hepatocellular Carcinoma by Regulating P21 via PI3K/AKT/GSK3β Pathway

Guo¹,

Ma²,

Wang³

et al. 2020

Preprint

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Background:Hepatocellular carcinoma (HCC) is a leading cancer worldwide for which diagnosis, treatment and progression are largely unknown. Keratin23 is a potential biomarker forHCC development; however, regulatory mechanisms underlying its expression remain unclear. Inthis research we explored the expression and effect of KRT23 underlying HCC development. Materials and methods:GEPIA was applied to analyze the expression of KRT23 in HCC samples and Kaplan-Merier survival analysis for patients’ prognosis. Next, IHC was further conducted for confirming its expression in HCC tissues. Meanwhile qRT-PCR and western blot analysis were applied to examine the expression of KRT23 on both mRNA and protein level in HCC cell lines compared with immortal hepatocyte LO2. Cell experiments including MTT assay, apoptosis analysis, cell cycle assay and clone formation assay were conducted for cell proliferation while transwell assay and scratch test for metastasis in vitro. Moreover, xenograft tumors in nude mice were further conducted for verification in vivo. As for mechanism in depth, immunofluorescence and western blot were operated to explore the effect of KRT23 on EMT and PI3K/AKT/GSK3βsignaling pathway. Furthermore, Co-immunoprecipitation was applied for interaction between KRT23 and P21. Functional rescue experiments were conducted to further testify their mutual effect.Results:For this research, we discovered the high expression of KRT23 in HCC samples and cell lines. Functionally, KRT23 knockdown reduced cell proliferation and metastasis in vitro and vivo. Furthermore, KRT23 participated in EMT progression and interacted with P21 to mediate PI3K/AKT/GSK3βpathway in HCC development.Conclusion:To summarize, KRT23 accelerated HCC proliferation and metastasis by regulating P21 via PI3K/AKT/GSK3βpathway.

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RBMS2 inhibits the proliferation by stabilizing P21 mRNA in breast cancer

Cited by 40 publications

References 33 publications

Knowdown of lncRNA HOXA-AS2 inhibits proliferation, invasion and migration of oral squamous cell carcinoma

Knowdown of lncRNA HOXA-AS2 inhibits proliferation, invasion and migration of oral squamous cell carcinoma

Oncogenic action of the exosome cofactor RBM7 by stabilization of CDK1 mRNA in breast cancer

KRT23 Acts as an Oncogene in Hepatocellular Carcinoma by Regulating P21 via PI3K/AKT/GSK3β Pathway

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