The microRNA signature of patients with sunitinib failure: regulation of <i>UHRF1</i> pathways by <i>microRNA-101</i> in renal cell carcinoma
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- Yusuke Goto
- Department of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan
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- Akira Kurozumi
- Department of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan
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- Nijiro Nohata
- Moores Cancer Center, University of California, San Diego, La Jolla, CA, United States of America
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- Satoko Kojima
- Department of Urology, Teikyo University Chiba Medical Center, Chiba, Japan
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- Ryosuke Matsushita
- Department of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan
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- Hirofumi Yoshino
- Department of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan
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- Kazuto Yamazaki
- Department of Pathology, Teikyo University Chiba Medical Center, Chiba, Japan
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- Yasuo Ishida
- Department of Pathology, Teikyo University Chiba Medical Center, Chiba, Japan
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- Tomohiko Ichikawa
- Department of Urology, Chiba University Graduate School of Medicine, Chiba, Japan
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- Yukio Naya
- Department of Urology, Teikyo University Chiba Medical Center, Chiba, Japan
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- Naohiko Seki
- Department of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan
書誌事項
- 公開日
- 2016-07-28
- 資源種別
- journal article
- DOI
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- 10.18632/oncotarget.10887
- 公開者
- Impact Journals, LLC
説明
Molecular targeted therapy is a standard treatment for patients with advanced renal cell carcinoma (RCC). Sunitinib is one of the most common molecular-targeted drugs for metastatic RCC. Molecular mechanisms of sunitinib resistance in RCC cells is still ambiguous. The microRNA (miRNA) expression signature of patients with sunitinib failure in RCC was constructed using a polymerase chain reaction (PCR)-based array. Several miRNAs that were aberrantly expressed in RCC tissues from patients treated with sunitinib were identified in this analysis. MicroRNA-101 (miR- 101) was markedly suppressed in sunitinib treated RCC tissues. Restoration of miR-101 significantly inhibited cell migration and invasion in Caki-1 and 786-O cells. Ubiquitin-like with PHD and ring finger domains 1 (UHRF1) was directly suppressed by miR-101 in RCC cells, and overexpression of UHRF1 was confirmed in sunitinib-treated RCC tissues. The pathways of nucleotide excision repair and mismatch repair were significantly suppressed by knockdown of UHRF1. Our findings showed that antitumor miR-101- mediated UHRF1 pathways may be suppressed by sunitinib treatment.
収録刊行物
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- Oncotarget
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Oncotarget 7 (37), 59070-59086, 2016-07-28
Impact Journals, LLC
