FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2326081853> ?p ?o ?g. }

• W2326081853 abstract "Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DCBackground: MicroRNAs are endogenous non-coding RNAs that can interfere with protein expression either by inducing the cleavage of specific target mRNAs or, in most cases, by inhibiting their translation. MicroRNA profiling studies using normal and cancer tissues suggested that a number of them are either overexpressed or down-regulated in tumors. Previously, we showed that miR-101 binds to a complementary sequence in the 3’UTR of EZH2, an oncogenic histone methyltransferase, and represses its expression. Our studies also demonstrated that ectopic miR-101 overexpression inhibits invasion of the aggressive prostate cell line DU145, and stable overexpression of miR-101 results in a reduction in tumor volume in vivo. Furthermore, we found that the genomic deletion of miR-101 during cancer progression leads to a concomitant increase in EZH2. COX2 is also a known target of miR-101 in colorectal cancers.Methods and Results: In the present study, bioinformatic analysis and functional studies revealed that miR-101 regulates multiple genes in prostate and breast cancer. Targets of miR-101 include oncoprotein STMN1 as well as Positive cofactor 4 (SUB1), a gene that is overexpressed in metastatic breast cancer. Investigation using 3’UTR luciferase reporter assays confirmed the regulation of these genes by miR-101. Furthermore, we validated the overexpression of STMN1 and SUB1 in aggressive prostate cancer by RTPCR and immunoblot analysis. We also demonstrated that ectopic overexpression of miR-101 in cancer cells down-regulated the expression of these genes. Immunohistochemical staining on prostate cancer tissue microarray representing aggressive and metastatic prostate cancer showed that STMN1 is highly expressed in metastatic prostate cancer. Tumor xenograft studies indicated that miR-101 target genes are involved in tumor growth. Together, these data identifies a critical tumor suppressive role for miR-101 and suggest that a loss of miR-101 in cancer leads to overexpression of multiple oncogenes.Conclusion: Overall, our studies indicate that miR-101 that is often down-regulated in multiple cancers due to genomic loss, acts as a master regulator of multiple oncogenes in cancer and reintroduction of miR-101 may have therapeutic benefit.Citation Format: Balabhadrapatruni V. S. K. Chakravarthi, Rohit Mehra, Rui Wang, Irfan A. Asangani, Qi Cao, Satya Pathi, Robert J. Lonigro, Christopher Maher, Daniel F. Camacho, Natalie McGregor, Nallasivam Palanisamy, Kenneth J. Pienta, Arul M. Chinnaiyan, Sooryanarayana Varambally. The role of microRNA-101 as a master tumor suppressor in cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4188. doi:10.1158/1538-7445.AM2013-4188" @default.
• W2326081853 created "2016-06-24" @default.
• W2326081853 creator A5003311852 @default.
• W2326081853 creator A5006531825 @default.
• W2326081853 creator A5016869947 @default.
• W2326081853 creator A5033907925 @default.
• W2326081853 creator A5042167871 @default.
• W2326081853 creator A5042516265 @default.
• W2326081853 creator A5046777605 @default.
• W2326081853 creator A5060849370 @default.
• W2326081853 creator A5070221783 @default.
• W2326081853 creator A5070812231 @default.
• W2326081853 creator A5077416434 @default.
• W2326081853 creator A5079699559 @default.
• W2326081853 creator A5087520734 @default.
• W2326081853 creator A5089377084 @default.
• W2326081853 date "2013-04-15" @default.
• W2326081853 modified "2023-09-22" @default.
• W2326081853 title "Abstract 4188: The role of microRNA-101 as a master tumor suppressor in cancer." @default.
• W2326081853 doi "https://doi.org/10.1158/1538-7445.am2013-4188" @default.
• W2326081853 hasPublicationYear "2013" @default.
• W2326081853 type Work @default.
• W2326081853 sameAs 2326081853 @default.
• W2326081853 citedByCount "0" @default.
• W2326081853 crossrefType "proceedings-article" @default.
• W2326081853 hasAuthorship W2326081853A5003311852 @default.
• W2326081853 hasAuthorship W2326081853A5006531825 @default.
• W2326081853 hasAuthorship W2326081853A5016869947 @default.
• W2326081853 hasAuthorship W2326081853A5033907925 @default.
• W2326081853 hasAuthorship W2326081853A5042167871 @default.
• W2326081853 hasAuthorship W2326081853A5042516265 @default.
• W2326081853 hasAuthorship W2326081853A5046777605 @default.
• W2326081853 hasAuthorship W2326081853A5060849370 @default.
• W2326081853 hasAuthorship W2326081853A5070221783 @default.
• W2326081853 hasAuthorship W2326081853A5070812231 @default.
• W2326081853 hasAuthorship W2326081853A5077416434 @default.
• W2326081853 hasAuthorship W2326081853A5079699559 @default.
• W2326081853 hasAuthorship W2326081853A5087520734 @default.
• W2326081853 hasAuthorship W2326081853A5089377084 @default.
• W2326081853 hasConcept C104317684 @default.
• W2326081853 hasConcept C121608353 @default.
• W2326081853 hasConcept C145059251 @default.
• W2326081853 hasConcept C153911025 @default.
• W2326081853 hasConcept C173396325 @default.
• W2326081853 hasConcept C2776438761 @default.
• W2326081853 hasConcept C2779723316 @default.
• W2326081853 hasConcept C2780192828 @default.
• W2326081853 hasConcept C502942594 @default.
• W2326081853 hasConcept C54355233 @default.
• W2326081853 hasConcept C555283112 @default.
• W2326081853 hasConcept C86803240 @default.
• W2326081853 hasConcept C97037327 @default.
• W2326081853 hasConceptScore W2326081853C104317684 @default.
• W2326081853 hasConceptScore W2326081853C121608353 @default.
• W2326081853 hasConceptScore W2326081853C145059251 @default.
• W2326081853 hasConceptScore W2326081853C153911025 @default.
• W2326081853 hasConceptScore W2326081853C173396325 @default.
• W2326081853 hasConceptScore W2326081853C2776438761 @default.
• W2326081853 hasConceptScore W2326081853C2779723316 @default.
• W2326081853 hasConceptScore W2326081853C2780192828 @default.
• W2326081853 hasConceptScore W2326081853C502942594 @default.
• W2326081853 hasConceptScore W2326081853C54355233 @default.
• W2326081853 hasConceptScore W2326081853C555283112 @default.
• W2326081853 hasConceptScore W2326081853C86803240 @default.
• W2326081853 hasConceptScore W2326081853C97037327 @default.
• W2326081853 hasLocation W23260818531 @default.
• W2326081853 hasOpenAccess W2326081853 @default.
• W2326081853 hasPrimaryLocation W23260818531 @default.
• W2326081853 hasRelatedWork W1251689262 @default.
• W2326081853 hasRelatedWork W1569658803 @default.
• W2326081853 hasRelatedWork W1939696168 @default.
• W2326081853 hasRelatedWork W1977745656 @default.
• W2326081853 hasRelatedWork W1990418200 @default.
• W2326081853 hasRelatedWork W2007193890 @default.
• W2326081853 hasRelatedWork W2012084030 @default.
• W2326081853 hasRelatedWork W2081742082 @default.
• W2326081853 hasRelatedWork W2312184723 @default.
• W2326081853 hasRelatedWork W2314938775 @default.
• W2326081853 hasRelatedWork W2317837188 @default.
• W2326081853 hasRelatedWork W2326685244 @default.
• W2326081853 hasRelatedWork W2330846224 @default.
• W2326081853 hasRelatedWork W2484648792 @default.
• W2326081853 hasRelatedWork W2489253307 @default.
• W2326081853 hasRelatedWork W2501732780 @default.
• W2326081853 hasRelatedWork W2520601168 @default.
• W2326081853 hasRelatedWork W2887366161 @default.
• W2326081853 hasRelatedWork W2894165877 @default.
• W2326081853 hasRelatedWork W3185315142 @default.
• W2326081853 isParatext "false" @default.
• W2326081853 isRetracted "false" @default.
• W2326081853 magId "2326081853" @default.
• W2326081853 workType "article" @default.