miR‐27 and miR‐124 target AR coregulators in prostate cancer: Bioinformatics and in vitro analysis
The inadequate efficacy of the current treatments for metastatic prostate cancer has directed efforts to the discovery of novel therapies. MicroRNAs (miRNAs) have been considered potential therapeutic agents due to their ability to control gene expression and cellular pathways. The accurate identifi...
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| Veröffentlicht in: | Andrologia 2022-10, Vol.54 (9), p.e14497-n/a |
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| creator | Jafari Najaf Abadi, Mohammad Hassan Khorashadizadeh, Mohsen Zarei Jaliani, Hossein Jamialahmadi, Khadigeh Aghaee‐Bakhtiari, Seyed Hamid |
| description | The inadequate efficacy of the current treatments for metastatic prostate cancer has directed efforts to the discovery of novel therapies. MicroRNAs (miRNAs) have been considered potential therapeutic agents due to their ability to control gene expression and cellular pathways. The accurate identification of genes and pathways which are targeted by a miRNA is the first step in the therapeutic use of these molecules. In this regard, there are multiple experimental and computational methods to predict and confirm the miRNA‐mRNA relationships. The targeting the androgen receptor (AR) indirectly as the most important mediator of prostate cancer has been posited to both control the disease and prevent resistance to treatment. This study aimed to identify miRNAs targeting AR coregulators. For this purpose, we examined target genes by combining miRNA‐mRNA computational and experimental data from various databases. miR‐27a‐3p and miR‐124 displayed the highest scores and were selected as miRNAs with the potential to target candidate genes. Next, three cell lines of prostate cancer including PC3, LNCAP, and DU145 were transfected with plasmids which were expressed these selected miRNAs. Then, the gene expression and cell cycle analysis were performed. A decrease was observed in cell viability in all three cell lines than the cells transfected with backbone plasmid. Furthermore, the findings indicated that miR‐27a‐3p and miR‐124 led to a significant decrease in the expression of all genes that were studied in PC3 cell line. In addition, miR‐124 caused significant the cellular arrest in the G0/G1 stage, while for miR‐27a‐3p, this arrest occurred was in the G2/M stage. Our results indicated that the function of a unique miRNA could be different in different cell lines with particular cancer phenotype based on the cell line stage. These findings offer the possibility of employing the miR‐124 and miR‐27a‐3p as therapeutic agents for prostate cancer treatment. |
| doi_str_mv | 10.1111/and.14497 |
| format | Article |
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MicroRNAs (miRNAs) have been considered potential therapeutic agents due to their ability to control gene expression and cellular pathways. The accurate identification of genes and pathways which are targeted by a miRNA is the first step in the therapeutic use of these molecules. In this regard, there are multiple experimental and computational methods to predict and confirm the miRNA‐mRNA relationships. The targeting the androgen receptor (AR) indirectly as the most important mediator of prostate cancer has been posited to both control the disease and prevent resistance to treatment. This study aimed to identify miRNAs targeting AR coregulators. For this purpose, we examined target genes by combining miRNA‐mRNA computational and experimental data from various databases. miR‐27a‐3p and miR‐124 displayed the highest scores and were selected as miRNAs with the potential to target candidate genes. Next, three cell lines of prostate cancer including PC3, LNCAP, and DU145 were transfected with plasmids which were expressed these selected miRNAs. Then, the gene expression and cell cycle analysis were performed. A decrease was observed in cell viability in all three cell lines than the cells transfected with backbone plasmid. Furthermore, the findings indicated that miR‐27a‐3p and miR‐124 led to a significant decrease in the expression of all genes that were studied in PC3 cell line. In addition, miR‐124 caused significant the cellular arrest in the G0/G1 stage, while for miR‐27a‐3p, this arrest occurred was in the G2/M stage. Our results indicated that the function of a unique miRNA could be different in different cell lines with particular cancer phenotype based on the cell line stage. These findings offer the possibility of employing the miR‐124 and miR‐27a‐3p as therapeutic agents for prostate cancer treatment.</description><identifier>ISSN: 0303-4569</identifier><identifier>EISSN: 1439-0272</identifier><identifier>DOI: 10.1111/and.14497</identifier><identifier>PMID: 35700742</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>androgen receptor ; Androgen receptors ; Bioinformatics ; Cell cycle ; Cell viability ; Computer applications ; coregulator ; Disease resistance ; Gene expression ; Metastases ; MicroRNAs ; miRNA ; Phenotypes ; Plasmids ; Prostate cancer ; therapeutic agent ; Tumor cell lines</subject><ispartof>Andrologia, 2022-10, Vol.54 (9), p.e14497-n/a</ispartof><rights>2022 Wiley‐VCH GmbH.</rights><rights>2022 Wiley-VCH GmbH.</rights><rights>2022 Wiley‐VCH GmbH</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3537-13580cb0f62cd3fd52b04b6e4c5da4438275c92f2968a29ee73bf7e2e2c93aa73</citedby><cites>FETCH-LOGICAL-c3537-13580cb0f62cd3fd52b04b6e4c5da4438275c92f2968a29ee73bf7e2e2c93aa73</cites><orcidid>0000-0002-6093-7837</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fand.14497$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fand.14497$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35700742$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jafari Najaf Abadi, Mohammad Hassan</creatorcontrib><creatorcontrib>Khorashadizadeh, Mohsen</creatorcontrib><creatorcontrib>Zarei Jaliani, Hossein</creatorcontrib><creatorcontrib>Jamialahmadi, Khadigeh</creatorcontrib><creatorcontrib>Aghaee‐Bakhtiari, Seyed Hamid</creatorcontrib><title>miR‐27 and miR‐124 target AR coregulators in prostate cancer: Bioinformatics and in vitro analysis</title><title>Andrologia</title><addtitle>Andrologia</addtitle><description>The inadequate efficacy of the current treatments for metastatic prostate cancer has directed efforts to the discovery of novel therapies. MicroRNAs (miRNAs) have been considered potential therapeutic agents due to their ability to control gene expression and cellular pathways. The accurate identification of genes and pathways which are targeted by a miRNA is the first step in the therapeutic use of these molecules. In this regard, there are multiple experimental and computational methods to predict and confirm the miRNA‐mRNA relationships. The targeting the androgen receptor (AR) indirectly as the most important mediator of prostate cancer has been posited to both control the disease and prevent resistance to treatment. This study aimed to identify miRNAs targeting AR coregulators. For this purpose, we examined target genes by combining miRNA‐mRNA computational and experimental data from various databases. miR‐27a‐3p and miR‐124 displayed the highest scores and were selected as miRNAs with the potential to target candidate genes. Next, three cell lines of prostate cancer including PC3, LNCAP, and DU145 were transfected with plasmids which were expressed these selected miRNAs. Then, the gene expression and cell cycle analysis were performed. A decrease was observed in cell viability in all three cell lines than the cells transfected with backbone plasmid. Furthermore, the findings indicated that miR‐27a‐3p and miR‐124 led to a significant decrease in the expression of all genes that were studied in PC3 cell line. In addition, miR‐124 caused significant the cellular arrest in the G0/G1 stage, while for miR‐27a‐3p, this arrest occurred was in the G2/M stage. Our results indicated that the function of a unique miRNA could be different in different cell lines with particular cancer phenotype based on the cell line stage. These findings offer the possibility of employing the miR‐124 and miR‐27a‐3p as therapeutic agents for prostate cancer treatment.</description><subject>androgen receptor</subject><subject>Androgen receptors</subject><subject>Bioinformatics</subject><subject>Cell cycle</subject><subject>Cell viability</subject><subject>Computer applications</subject><subject>coregulator</subject><subject>Disease resistance</subject><subject>Gene expression</subject><subject>Metastases</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Phenotypes</subject><subject>Plasmids</subject><subject>Prostate cancer</subject><subject>therapeutic agent</subject><subject>Tumor cell lines</subject><issn>0303-4569</issn><issn>1439-0272</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp1kMtKxDAUhoMozqCz8AUk4EYX1eQkaVp343gFURh0XdI0HSK9aNIqs_MRfEafxDgdXQj-m8OBj49zfoT2KDmmISeqKY4p56ncQGPKWRoRkLCJxoQRFnERpyM08f6JhHAhJefbaMSEJERyGKOytvPP9w-QOHjwsFDguFNuYTo8nWPdOrPoK9W1zmPb4GfX-k51BmvVaONO8ZltbVO2rlad1X7lCdir7VwbFlUtvfW7aKtUlTeT9dxBj5cXD7Pr6Pb-6mY2vY00E0xGlImE6JyUMeiClYWAnPA8NlyLQnHOEpBCp1BCGicKUmMky0tpwIBOmVKS7aDDwRuufOmN77Laem2qSjWm7X0GsYxTEBSSgB78QZ_a3oV7AyVJkiTAKQ3U0UDp8LZ3psyena2VW2aUZN_9Z-HfbNV_YPfXxj6vTfFL_rQdgJMBeLOVWf5vyqZ354PyC1fgjt4</recordid><startdate>202210</startdate><enddate>202210</enddate><creator>Jafari Najaf Abadi, Mohammad Hassan</creator><creator>Khorashadizadeh, Mohsen</creator><creator>Zarei Jaliani, Hossein</creator><creator>Jamialahmadi, Khadigeh</creator><creator>Aghaee‐Bakhtiari, Seyed Hamid</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6093-7837</orcidid></search><sort><creationdate>202210</creationdate><title>miR‐27 and miR‐124 target AR coregulators in prostate cancer: Bioinformatics and in vitro analysis</title><author>Jafari Najaf Abadi, Mohammad Hassan ; Khorashadizadeh, Mohsen ; Zarei Jaliani, Hossein ; Jamialahmadi, Khadigeh ; Aghaee‐Bakhtiari, Seyed Hamid</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3537-13580cb0f62cd3fd52b04b6e4c5da4438275c92f2968a29ee73bf7e2e2c93aa73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>androgen receptor</topic><topic>Androgen receptors</topic><topic>Bioinformatics</topic><topic>Cell cycle</topic><topic>Cell viability</topic><topic>Computer applications</topic><topic>coregulator</topic><topic>Disease resistance</topic><topic>Gene expression</topic><topic>Metastases</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Phenotypes</topic><topic>Plasmids</topic><topic>Prostate cancer</topic><topic>therapeutic agent</topic><topic>Tumor cell lines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jafari Najaf Abadi, Mohammad Hassan</creatorcontrib><creatorcontrib>Khorashadizadeh, Mohsen</creatorcontrib><creatorcontrib>Zarei Jaliani, Hossein</creatorcontrib><creatorcontrib>Jamialahmadi, Khadigeh</creatorcontrib><creatorcontrib>Aghaee‐Bakhtiari, Seyed Hamid</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Andrologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jafari Najaf Abadi, Mohammad Hassan</au><au>Khorashadizadeh, Mohsen</au><au>Zarei Jaliani, Hossein</au><au>Jamialahmadi, Khadigeh</au><au>Aghaee‐Bakhtiari, Seyed Hamid</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR‐27 and miR‐124 target AR coregulators in prostate cancer: Bioinformatics and in vitro analysis</atitle><jtitle>Andrologia</jtitle><addtitle>Andrologia</addtitle><date>2022-10</date><risdate>2022</risdate><volume>54</volume><issue>9</issue><spage>e14497</spage><epage>n/a</epage><pages>e14497-n/a</pages><issn>0303-4569</issn><eissn>1439-0272</eissn><abstract>The inadequate efficacy of the current treatments for metastatic prostate cancer has directed efforts to the discovery of novel therapies. MicroRNAs (miRNAs) have been considered potential therapeutic agents due to their ability to control gene expression and cellular pathways. The accurate identification of genes and pathways which are targeted by a miRNA is the first step in the therapeutic use of these molecules. In this regard, there are multiple experimental and computational methods to predict and confirm the miRNA‐mRNA relationships. The targeting the androgen receptor (AR) indirectly as the most important mediator of prostate cancer has been posited to both control the disease and prevent resistance to treatment. This study aimed to identify miRNAs targeting AR coregulators. For this purpose, we examined target genes by combining miRNA‐mRNA computational and experimental data from various databases. miR‐27a‐3p and miR‐124 displayed the highest scores and were selected as miRNAs with the potential to target candidate genes. Next, three cell lines of prostate cancer including PC3, LNCAP, and DU145 were transfected with plasmids which were expressed these selected miRNAs. Then, the gene expression and cell cycle analysis were performed. A decrease was observed in cell viability in all three cell lines than the cells transfected with backbone plasmid. Furthermore, the findings indicated that miR‐27a‐3p and miR‐124 led to a significant decrease in the expression of all genes that were studied in PC3 cell line. In addition, miR‐124 caused significant the cellular arrest in the G0/G1 stage, while for miR‐27a‐3p, this arrest occurred was in the G2/M stage. Our results indicated that the function of a unique miRNA could be different in different cell lines with particular cancer phenotype based on the cell line stage. 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| subjects | androgen receptor Androgen receptors Bioinformatics Cell cycle Cell viability Computer applications coregulator Disease resistance Gene expression Metastases MicroRNAs miRNA Phenotypes Plasmids Prostate cancer therapeutic agent Tumor cell lines |
| title | miR‐27 and miR‐124 target AR coregulators in prostate cancer: Bioinformatics and in vitro analysis |
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