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• W2145632098 abstract "// Dong Hyun Jo 1, 2, 3 , Jin Hyoung Kim 1, 2 , Chang Sik Cho 1, 2, 3 , Young-Lai Cho 4 , Hyoung Oh Jun 1, 2 , Young Suk Yu 1, 5 , Jeong-Ki Min 6 , Jeong Hun Kim 1, 2, 3, 5 1 Fight against Angiogenesis-Related Blindness (FARB) Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea 2 Tumor Microenvironment Research Center, Global Core Research Center, Seoul National University, Seoul, Republic of Korea 3 Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Republic of Korea 4 Center for Nanosafety Metrology, Korea Research Institute of Standards and Science Daejeon, Republic of Korea 5 Department of Ophthalmology, College of Medicine, Seoul National University, Seoul, Republic of Korea 6 Research Center for Integrated Cellulomics, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea Correspondence to: Jeong Hun Kim, e-mail: steph25@snu.ac.kr Jeong-Ki Min, e-mail: jekmin@kribb.re.kr Keywords: Retinoblastoma, STAT3 transcription factor, miR-17-92 Received: July 12, 2014      Accepted: September 30, 2014      Published: November 03, 2014 ABSTRACT Retinoblastoma, the most common intraocular malignant tumor in children, is characterized by the loss of both functional alleles of RB1 gene, which however alone cannot maintain malignant characteristics of retinoblastoma cells. Nevertheless, the investigation of other molecular aberrations such as matrix metalloproteinases (MMPs) and miRNAs is still lacking. In this study, we demonstrate that STAT3 is activated in retinoblastoma cells, Ki67-positive areas of in vivo orthotopic tumors in BALB/c nude mice, and human retinoblastoma tissues of the advanced stage. Furthermore, target genes of STAT3 including BCL2 , BCL2L1 , BIRC5 , and MMP9 are up-regulated in retinoblastoma cells compared to other retinal constituent cells. Interestingly, STAT3 inhibition by targeted siRNA suppresses the proliferation of retinoblastoma cells and the formation of in vivo orthotopic tumors. In line with these results, STAT3 siRNA effectively induces down-regulation of target genes of STAT3. In addition, miRNA microarray analysis and further real-time PCR experiments with STAT3 siRNA treatment show that STAT3 activation is related to the up-regulation of miR-17-92 clusters in retinoblastoma cells via positive feedback loop between them. In conclusion, we suggest that STAT3 inhibition could be a potential therapeutic approach in retinoblastoma through the suppression of tumor proliferation." @default.
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• W2145632098 date "2014-11-03" @default.
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• W2145632098 title "STAT3 inhibition suppresses proliferation of retinoblastoma through down-regulation of positive feedback loop of STAT3/miR-17-92 clusters" @default.
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• W2145632098 doi "https://doi.org/10.18632/oncotarget.2546" @default.
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