MicroRNA-34 mediates AR-dependent p53-induced apoptosis in prostate cancer

Rokhlin, Oskar W.; Scheinker, Vladimir; Taghiyev, Agshin F.; Bumcrot, David; Glover, Rebecca A.; Cohen, Michael B.

doi:10.4161/cbt.7.8.6284

Cited by 140 publications

(103 citation statements)

References 33 publications

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“…In addition, Myc could interact with miR-34b directly in the present study. miR-34 mediates androgen receptor-dependent p53-induced apoptosis in prostate cancer (39). The study by Corney et al confirmed that miR-34b Term, identification number of GO term or KEGG pathway; Description, name of GO term or KEGG pathway; Count, number of genes enriched in GO term or KEGG pathway.…”

Section: Discussionmentioning

confidence: 91%

Signal transduction by M3 muscarinic acetylcholine receptor in prostate cancer

et al. 2015

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Abstract. The present study aimed to investigate the potential mechanisms used during signal transduction by M3 muscarinic acetylcholine receptor (CHRM3) in prostate cancer. The microarray datasets of GSE3325, including 5 clinically localized primary prostate cancers and 4 benign prostate tissues, were downloaded from the Gene Expression Omnibus database. The differentially-expressed genes (DEGs) in primary prostate cancer tissues compared with benign controls were screened using the Limma package. Gene Ontology and pathway enrichment analyses were performed using the Database for Annotation Visualization and Integrated Discovery. Next, a protein-protein interaction (PPI) network was constructed. Additionally, microRNAs (miRNAs) associated with DEGs were predicted and miRNA-target DEG analysis was performed using a Web-based Gene Set Analysis Toolkit. Finally, the PPI network and the miRNA-target DEG network were integrated using Cytoscape. In total, 224 DEGs were screened in the prostate cancer tissues, including 113 upregulated and 111 downregulated genes. CHRM3 and epidermal growth factor (EGF) were enriched in the regulation of the actin cytoskeleton. EGF and v-myc avian myelocytomatosis viral oncogene homolog (Myc) were enriched in the mitogen-activated protein kinase (MAPK) signaling pathway. EGF with the highest degree of connectivity was the hub node in the PPI network, and miR-34b could interact with Myc directly in the miRNA-target DEG network. EGF and Myc may exhibit significant roles in the progression of prostate cancer via regulation of the actin cytoskeleton and the MAPK signaling pathway. CHRM3 may activate these two pathways in prostate cancer progression. Thus, these two key factors and pathways may be crucial mechanisms during signal transduction by CHRM3 in prostate cancer. IntroductionProstate cancer is one of the leading causes of cancer-associated mortality in males, accounting for >240,000 new cancer cases and 28,000 fatalities annually in males in the United States (1,2). Although effective surgical and radiation treatments exist for clinically localized prostate cancer, the majority of patients with metastatic prostate cancer eventually succumb to the disease (3). Therefore, in order to develop more effective outcomes for the diagnosis and treatment of prostate cancer, articulation of the genetic underpinning and novel therapeutic targets are critically required.Recently, the presence and function of muscarinic acetylcholine receptors (mAChRs) in the human prostate have aroused wide concern (4,5). mAChR and its ligands have been found to play key roles in regulating cellular proliferation and cancer progression (6). mAChRs are preferentially localized to the glandular epithelium of the prostate and promote the paracrine/autocrine actions within the prostate gland, which are critical for cancer cell survival, proliferation and migration (4,6,7). mAChRs consist of five distinct subtypes (M1-M5), and the M3 mAChR (also known as CHRM3) has been found to be a key member involved in prostate ...

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Section: Discussionmentioning

confidence: 91%

Signal transduction by M3 muscarinic acetylcholine receptor in prostate cancer

et al. 2015

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“…Nevertheless, it is mandatory to validate the expression of reference genes for each study design, as normalization to an unsuitable reference gene has been shown to lead to biased results (Dheda et al, 2005;Ohl et al, 2005). In the majority of miRNA expression studies, miRNAs or other small RNAs were used as reference genes, but some studies also normalized expression to longer mRNAs, namely GAPDH, TATA box binding protein mRNA, and RNAseP (Porkka et al, 2007;Huang et al, 2008;Place et al, 2008;Rokhlin et al, 2008;Gandellini et al, 2009). It is questionable as to whether mRNAs can be used as reference genes in miRNA expression studies, because longer RNAs may have different isolation efficiencies compared to miRNAs (Peltier and Latham, 2008), they may be degraded faster due to their length, and they are reverse transcribed with different techniques than the miRNAs of interest.…”

Section: Discussionmentioning

confidence: 99%

“…We identified 16 articles (Jiang et al, 2005;Mattie et al, 2006;Porkka et al, 2007;Ambs et al, 2008;Josson et al, 2008;Mitchell et al, 2008;Ozen et al, 2008;Place et al, 2008;Prueitt et al, 2008;Rokhlin et al, 2008;Gandellini et al, 2009;Leite et al, 2009;Noonan et al, 2009;Siva et al, 2009;Spahn et al, 2009;Tong et al, 2009), in which miRNA RT-qPCR was performed. In 14 articles, relative quantification was performed and the reference genes utilized were specified.…”

Section: Introductionmentioning

confidence: 99%

“…The most commonly used reference gene was the small RNA RNU6-2 which was used in 4 studies (Jiang et al, 2005;Prueitt et al, 2008;Noonan et al, 2009). Further reference genes or combination of reference genes were: GAPDH (Place et al, 2008;Rokhlin et al, 2008) and RNU6-2/SNORD43 (Ozen et al, 2008;Spahn et al, 2009) (each twice), SNORD43 (Leite et al, 2009), TATA box binding protein mRNA (Porkka et al, 2007), RNU6-2/miR-16 (Josson et al, 2008), RNU6-2/RNaseP (Gandellini et al, 2009), and let-7/miR-16 (Mattie et al, 2006) (each once). The reasons for selection of the reference genes were only given in three studies, but these were not satisfying (Jiang et al, 2005;Mattie et al, 2006;Josson et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

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Suitable reference genes for relative quantification of miRNA expression in prostate cancer

et al. 2010

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Real time quantitative PCR (qPCR) is the method of choice for miRNA expression studies. For relative quantification of miRNAs, normalization to proper reference genes is mandatory. Currently, no validated reference genes for miRNA qPCR in prostate cancer are available. In this study, the expression of four putative reference genes (hsa-miR-16, hsa-miR-130b, RNU6-2, SNORD7) was examined with regard to their use as normalizer. After SNORD7 was already shown an inappropriate reference gene in preliminary experiments using total RNA pools, we studied the expression of the putative reference genes in tissue and normal adjacent tissue sample pairs from 76 men with untreated prostate carcinoma collected after radical prostatectomy. hsa-miR-130b and RNU6-2 showed no significantly different expression between the matched malignant and non-malignant tissue samples, whereas hsa-miR-16 was significantly underexpressed in malignant tissue. Softwares geNorm and Normfinder predicted hsamiR-130b and the geometric mean of hsa-miR-130b and RNU6-2 as the most stable reference genes. Normalization of the four miRNAs hsa-miR-96, hsamiR-125b, hsa-miR-205, and hsa-miR-375, which were previously shown to be regulated, shows that normalization to hsa-mir-16 can lead to biased results. We recommend using hsa-miR-130b or the geometric mean of hsa-miR-130b and small RNA RNU6-2 for normalization in miRNA expression studies of prostate cancer.

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“…miRNA-based treatment for human tumors has been documented extensively. The tumor suppressor role of mir-34 has been confirmed in vivo with these tumor xenografts via activation of the p53 pathway (16). The use of locked nucleic acid anti-mir-21 oligonucleotides has been reported to reduce the growth of U87 glioblastoma xenograft by >70% (17).…”

Section: Introductionmentioning

confidence: 92%

Tumor-suppressive mir-663 gene induces mitotic catastrophe growth arrest in human gastric cancer cells

Pan

Hu²,

Zhou³

et al. 2010

Oncol Rep

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Abstract. Increasing evidence suggests that microRNAs are involved in human carcinogenesis as tumor suppressors or oncogenes. A growing number of reports has shown that an interest has been sparked in aberrant microRNA expression and how they can be used to treat human diseases, including cancer. However, their precise biological role remains largely unknown. In the present study, we aimed to identify micro-RNA species involved in the regulation of tumor growth. By performing quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis, we demonstrated that mir-663 was downregulated in human gastric cancer cell lines unlike in normal cells. A transient introduction of mir-663 into the human gastric cancer cell lines BGC823 and SNU5 induced morphology changes and suppression of proliferation of these cells. In addition, mir-663 alters the DNA content and induces phenotypes of mitotic catastrophe in tumor cells. Moreover, the liposome-mediated delivery of mir-663 suppressed the in vivo growth of the BGC823 and SNU5 cells. Western blot analyses performed after the introduction of mir-663 revealed upregulation of cyclin B following transfection with mir-663. Our results provide evidence that downregulation of mir-663 in tumor cells may contribute to aberrant cell hyperplasia, leading to the development of gastric cancer. Therefore, mir-663 might function as a potent suppressor of tumor growth.

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MicroRNA-34 mediates AR-dependent p53-induced apoptosis in prostate cancer

Cited by 140 publications

References 33 publications

Signal transduction by M3 muscarinic acetylcholine receptor in prostate cancer

Signal transduction by M3 muscarinic acetylcholine receptor in prostate cancer

Suitable reference genes for relative quantification of miRNA expression in prostate cancer

Tumor-suppressive mir-663 gene induces mitotic catastrophe growth arrest in human gastric cancer cells

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