CREB5 promotes tumor cell invasion and correlates with poor prognosis in epithelial ovarian cancer

He, Shanyang; Deng, Ying; Liao, Yanbin; Li, Xiaojin; Li, Jun; Yao, Shuzhong

doi:10.3892/ol.2017.7234

Cited by 25 publications

(33 citation statements)

References 22 publications

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“…Transcriptome analysis showed that dysregulation of genes associated with cell invasion and immunity might contribute to idiopathic RPL [ 31 ]. CREB5 gene, belonging to the CRE (cAMP response element)-binding protein family, has crucial roles in regulating cell growth, proliferation, differentiation and cell cycle [ 32 , 33 ]. Recently, relevant studies have suggested that the up-regulation of CREB5 is negatively correlated with the prognosis of epithelial ovarian cancer and non-small cell lung cancer and accelerate the metastasis of cancers [ 33 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

“…CREB5 gene, belonging to the CRE (cAMP response element)-binding protein family, has crucial roles in regulating cell growth, proliferation, differentiation and cell cycle [ 32 , 33 ]. Recently, relevant studies have suggested that the up-regulation of CREB5 is negatively correlated with the prognosis of epithelial ovarian cancer and non-small cell lung cancer and accelerate the metastasis of cancers [ 33 , 34 ]. In addition, modifications of CREB5 methylation and expression were reported to be associated with plasma interleukin-6 (IL-6) levels and map to the network of inflammatory response genes [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

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Integrated analysis of DNA methylome and transcriptome identified CREB5 as a novel risk gene contributing to recurrent pregnancy loss

et al. 2018

EBioMedicine

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Background Aberrant DNA methylation is considered to be a potential cause of recurrent pregnancy loss (RPL), while potential mechanism has not yet been elucidated. Methods In order to uncover the contribution of the perturbation of DNA methylation in RPL, we performed genome-wide DNA methylation analysis combined with genome-wide gene expression in decidua tissue. Findings Totally, 539 differentially methylated regions (DMRs) were identified and significantly correlated with gene expressions. We observed that hypo-methylated DMR near CREB5 recruited transcription factors binding, such as P53 and SP1, and in turn upregulated CREB5. Compromised cell migration and apoptosis were observed in human CREB5 overexpression trophoblast cell lines, indicating dysfunctional trophoblast cells might contribute to RPL after hypo-methylation of CREB5 . In addition, overexpression of CREB5 altered cell cycle. Interpretation Our data highlights a role of CREB5 involved in the pathogenesis of RPL, and CREB5 maybe a potential diagnostic biomarker for RPL.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Integrated analysis of DNA methylome and transcriptome identified CREB5 as a novel risk gene contributing to recurrent pregnancy loss

et al. 2018

EBioMedicine

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“…Examination of TCGA pan cancer datasets revealed frequent CREB5 amplification and overexpression in kidney cancers, sarcomas, lymphomas, and lung adenocarcinomas as well as glioblastomas and gliomas [10]. Experimental investigations showed that CREB5 was upregulated in ovarian cancers [11], hepatocellular carcinoma [12], and prostate cancer [10]. High CREB5 expression correlated with a poor prognosis in epithelial ovarian cancer [11] and hepatocellular carcinoma [12].…”

Section: Introductionmentioning

confidence: 99%

CREB5 promotes invasiveness and metastasis in colorectal cancer by directly activating MET

Wang

Qiu

Liu

et al. 2020

J Exp Clin Cancer Res

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Background: cAMP responsive element binding protein 5 (CREB5) is a transcriptional activator in eukaryotic cells that can regulate gene expression. Previously, we found that CREB5 was involved in the occurrence and development of colorectal cancer (CRC) using bioinformatics analysis. However, the biological roles and underlying regulatory mechanism of CREB5 in CRC remain unclear. Methods: Real-time PCR, western blotting, and immunohistochemistry were used to examine CREB5 expression. In vitro experiments including migration assay, wound-healing assay, chicken chorioallantoic membrane assay, and human umbilical vein endothelial cells tube formation assay were used to investigate the effects of CREB5 on CRC cell migration and tumor angiogenesis ability. Additionally, an orthotopic implantation assay was performed in nude mice to confirm the effects of CREB5 in vivo. Furthermore, gene set enrichment analysis was performed to explore the potential mechanism of CREB5 in CRC. Results: We found that CREB5 expression was highly upregulated in CRC. CREB5 overexpression was positively correlated with advanced WHO stages and TNM stages and shorter survival in CRC patients. Moreover, CREB5 overexpression promoted while CREB5 silencing reduced the invasiveness and metastatic capacity of CRC cells both in vitro and in vivo. Furthermore, CREB5 directly interacted with the MET promoter and activated the hepatocyte growth factor-MET signalling pathway. Importantly, inhibition of MET reduced the invasion and metastasis of CREB5-overexpressing CRC cells, suggesting that CREB5 promotes metastasis mainly through activation of MET signalling. Conclusion: Our study demonstrates a crucial role for CREB5 in CRC metastasis by directly upregulating MET expression. CREB5 may be both a potential prognostic marker and a therapeutic target to effectively overcome metastasis in CRC.

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“…For example, when CREB5 was overexpressed, it up-regulates CSF1R, MMP9, PDGFRB, FIGF, and IL6 to promote metastasis of colorectal cancer [20]. In addition, when CREB5 expression is higher in patients with the epithelial ovarian cancer, their survival rate and the no-recurrence rates are low [21]. Some studies have shown that CREB5 is a negative regulator of viral infection.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA 876-5p modulates EV-A71 replication through downregulation of host antiviral factors

Cheng

et al. 2020

Virol J

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Background: Human enterovirus 71 (EV-A71) is a non-enveloped virus that has a single stranded positive sense RNA genome. In a previous study, we showed that miR-876-5p upregulation was observed in the serum of patients with severe EV-A71 infection. Micro-876-5p (miR-876-5p) is a circulating miRNA that can be identified to modulate EV-A71 infections through both in vitro and in vivo studies. However, the regulatory mechanisms that involve miR-876-5p in the EV-A71 infection cycle remain unclear. Methods: We demonstrated that miR-876-5p facilitated EV-A71 replication and expression by overexpression and knocking-down of miR-876-5p through the transfection of miR-876-5p plasmid and miR-876-5p inhibitor. Although miR-876-5p suppressed CREB5 expression, luciferase reporter assay confirmed this. We also evaluated the role of miR-876-5p in the EV-A71 infection cycle by CREB5 mediated by transfection with an anti-miR-876-5P inhibitor or in combination with an si-CREB5 plasmid. Results: MicroR-876-5p was upregulated in EV-A71-infected neuroblastoma cells. Overexpression of miR-876-5p or knockdown of cyclic-AMP responsive element binding protein 5 (CREB5) promoted EV-A71 replication. The downregulation of miR-876-5p inhibited the accumulation of viral RNA and the production of viral proteins. Interestingly, CREB5 overexpression also suppressed EV-A71 replication. Our in vitro studies reveal that miR-876-5p directly targets CREB5. Finally, downregulation of CREB5 protein abated the inhibitory effect of anti-miR-876-5p and induced inhibitory effect of EV-A71 replication. Conclusions: Our results suggest that intracellular miR-876-5p promotes EV-A71 replication indirectly by targeting the host CREB5 protein.

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CREB5 promotes tumor cell invasion and correlates with poor prognosis in epithelial ovarian cancer

Cited by 25 publications

References 22 publications

Integrated analysis of DNA methylome and transcriptome identified CREB5 as a novel risk gene contributing to recurrent pregnancy loss

Integrated analysis of DNA methylome and transcriptome identified CREB5 as a novel risk gene contributing to recurrent pregnancy loss

CREB5 promotes invasiveness and metastasis in colorectal cancer by directly activating MET

MicroRNA 876-5p modulates EV-A71 replication through downregulation of host antiviral factors

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