Identification of ZNF217, hnRNP‐K, VEGF‐A and IPO7 as targets for microRNAs that are downregulated in prostate carcinoma

Szczyrba, Jaroslaw; Nolte, Elke; Hart, Martin; Döll, Celina; Wach, Sven; Täubert, Helge; Keck, Bastian; Kremmer, Elisabeth; Stöhr, Robert; Hartmann, Arndt; Wullich, Bernd; Grässer, Friedrich A.

doi:10.1002/ijc.27731

Cited by 65 publications

(61 citation statements)

References 45 publications

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“…Analyses of prostate tissue and cell lines have identified multiple miRNAs, the expressions of which are consistently being altered in prostate tumors, which has led to further analysis of downstream gene targets and their potential contribution to carcinogenesis. Szczyrba et al (2010Szczyrba et al ( , 2013 reported a significant reduction of miR-29b expression in PCa and subsequently demonstrated miR-29b as a direct regulator of VEGF in PCa cell lines LNCaP and DU145. In addition to miR-29b, the VEGF transcript is predicted to contain binding sites for multiple miRNA types (as highlighted in Fig.…”

Section: Post-transcriptional Regulation Of Vegf Signaling In Pcamentioning

confidence: 95%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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Prostate cancer (PCa) is the most common malignancy affecting men in the western world. Although radical prostatectomy and radiation therapy can successfully treat PCa in the majority of patients, up to w30% will experience local recurrence or metastatic disease. Prostate carcinogenesis and progression is typically an androgen-dependent process. For this reason, therapies for recurrent PCa target androgen biosynthesis and androgen receptor function. Such androgen deprivation therapies (ADT) are effective initially, but the duration of response is typically %24 months. Although ADT and taxane-based chemotherapy have delivered survival benefits, metastatic PCa remains incurable. Therefore, it is essential to establish the cellular and molecular mechanisms that enable localized PCas to invade and disseminate. It has long been accepted that metastases require angiogenesis. In the present review, we examine the essential role for angiogenesis in PCa metastases, and we focus in particular on the current understanding of the regulation of vascular endothelial growth factor (VEGF) in localized and metastatic PCa. We highlight recent advances in understanding the role of VEGF in regulating the interaction of cancer cells with tumor-associated immune cells during the metastatic process of PCa. We summarize the established mechanisms of transcriptional and post-transcriptional regulation of VEGF in PCa cells and outline the molecular insights obtained from preclinical animal models of PCa. Finally, we summarize the current state of anti-angiogenesis therapies for PCa and consider how existing therapies impact VEGF signaling.

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Section: Post-transcriptional Regulation Of Vegf Signaling In Pcamentioning

confidence: 95%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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“…It can inhibit or promote tumor formation depending on its binding targets and microenvironment. Furthermore, it was found that miR-205 can bind to the 3'UTR of hnRNP K to reduce hnRNP K expression (50). However, miR-205 is downregulated in prostate cancer, so its inhibition for hnRNP K is derepressed, which leads to promoting the state of tumors (51).…”

Section: Hnrnp K Interacts With Non-coding Rnas (Ncrnas) To Promote Tmentioning

confidence: 98%

Role and molecular mechanism of heterogeneous nuclear ribonucleoprotein K in tumor development and progression

Gao

2016

Biomedical Reports

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Heterogeneous nuclear ribonucleoprotein K (hnRNP K) is a member of the hnRNP family, which exists in the nucleus and the cytoplasm simultaneously. It is a multifunctional protein that can participate in a variety of regulatory progressions of gene expression and signal transduction, such as chromatin remodeling, transcription, RNA alternative splicing and translation. hnRNP K not only directly binds to the kinases, but also recruits the associated factors regarding transcription, splicing and translation to control gene expression, and therefore, it serves as a docking platform for integrating transduction pathways to nucleic acid-directed processes. Numerous studies also show that abnormal expression of hnRNP K is closely associated with the tumor formation. This protein is overexpressed in numerous types of cancer and its aberrant cytoplasmic localization is also associated with a worse prognosis for patients. These results consistently indicate that hnRNP K has a key role in cancer progression. To understand the hnRNP K pathophysiological process in tumor disease, the previous research results regarding the association between hnRNP K and tumors were reviewed.

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“…Although cancer-specific alternative splicing in prostate cancer is a well-known process [27], we can only speculate about the regulation of alternative splicing of ERG. We have previously shown that one [28]. By interacting with hnRNP-L [29], over-expression of hnRNP-K may influence alternative splicing via interaction with intronic splice silencer or splice enhancer sequences [30].…”

Section: Discussionmentioning

confidence: 99%

The proto‐oncogeneERGis a target of microRNAmiR‐145in prostate cancer

et al. 2013

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Prostate cancer is a leading cause of cancer mortality in men. One of the distinct characteristics of prostate cancer is over-expression of the ERG proto-oncogene. The TMPRSS2-ERG gene fusion, the most common gene fusion, is found in approximately 50% of prostate cancer cases. We show that certain microRNAs are extensively deregulated in prostate cancer cell lines and primary clinical cancer samples. MicroRNAs are capable of modulating post-transcriptional gene expression via inhibition of protein synthesis. Independent target prediction methods have indicated that the 3′ untranslated region of the ERG mRNA is a potential target of miR-145. miR-145 is consistently down-regulated in prostate cancer. Here we show that the ERG 3′ untranslated region is a regulative target of miR-145 in vitro. Ectopic expression of miR-145 led to a reduction in expression of the ERG protein. We analyzed 26 prostate cancer samples and corresponding normal tissue. ERG protein expression was found to be elevated in the tumor samples, together with increased expression of several ERG isoforms. We identified ERG proteins of 35 and 24 kDa, which may represent unknown ERG splice variants. Analyses of miR-145 and ERG mRNA expression revealed a general down-regulation of miR-145 irrespective of the presence or absence of translocations involving ERG. This observation indicates that down-regulation of miR-145 may contribute to the increased expression of most ERG splice variants sharing the miR-145 target sequence in their 3′ untranslated region.

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Identification of ZNF217, hnRNP‐K, VEGF‐A and IPO7 as targets for microRNAs that are downregulated in prostate carcinoma

Cited by 65 publications

References 45 publications

Regulation of vascular endothelial growth factor in prostate cancer

Regulation of vascular endothelial growth factor in prostate cancer

Role and molecular mechanism of heterogeneous nuclear ribonucleoprotein K in tumor development and progression

The proto‐oncogeneERGis a target of microRNAmiR‐145in prostate cancer

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