Upregulation of miR-489-3p and miR-630 inhibits oxaliplatin uptake in renal cell carcinoma by targeting OCT2

Renal cell carcinoma (RCC) is one of the most common malignant tumors affecting the urogenital system, accounting for 90% of renal malignancies. Traditional chemotherapy options are often the front-line choice of regimen in the treatment of patients with RCC, but responses may be modest or limited d...

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Published inActa pharmaceutica Sinica. B Vol. 9; no. 5; pp. 1008 - 1020
Main Authors Chen, Lu, Chen, Le, Qin, Zhiyuan, Lei, Jinxiu, Ye, Sheng, Zeng, Kui, Wang, Hua, Ying, Meidan, Gao, Jianqing, Zeng, Su, Yu, Lushan
Format Journal Article
LanguageEnglish
Published Elsevier 01.09.2019
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Abstract Renal cell carcinoma (RCC) is one of the most common malignant tumors affecting the urogenital system, accounting for 90% of renal malignancies. Traditional chemotherapy options are often the front-line choice of regimen in the treatment of patients with RCC, but responses may be modest or limited due to resistance of the tumor to anticarcinogen. Downregulated expression of organic cation transporter OCT2 is a possible mechanism underlying oxaliplatin resistance in RCC treatment. In this study, we observed that miR-489-3p and miR-630 suppress OCT2 expression by directly binding to the OCT2 3′-UTR. Meanwhile, via 786-O-OCT2-miRNAs stable expression cell models, we found that miRNAs could repress the classic substrate 1-methyl-4-phenylpyridinium (MPP + ), fluorogenic substrate N , N -dimethyl-4-(2-pyridin-4-ylethenyl) aniline (ASP + ), and oxaliplatin uptake by OCT2 both in vitro and in xenografts. In 33 clinical samples, miR-489-3p and miR-630 were significantly upregulated in RCC, negatively correlating with the OCT2 expression level compared to that in adjacent normal tissues, using tissue microarray analysis and qPCR validation. The increased binding of c-Myc to the promoter of pri-miR-630, responsible for the upregulation of miR-630 in RCC, was further evidenced by chromatin immunoprecipitation and dual-luciferase reporter assay. Overall, this study indicated that miR-489-3p and miR-630 function as oncotherapy-obstructing microRNAs by directly targeting OCT2 in RCC. MiR-489-3p, c-Myc and miR-630 mediate OCT2 downregulation in RCC cells. MiR-489-3p and miR-630 is abnormally upregulated in RCC samples and exosomes, suppressing OCT2 expression by directly binding to the OCT2 3′-UTR. The increased binding of c-Myc to the promoter of pri-miR-630, contributes to the upregulation of miR-630 in RCC. fx1
AbstractList Renal cell carcinoma (RCC) is one of the most common malignant tumors affecting the urogenital system, accounting for 90% of renal malignancies. Traditional chemotherapy options are often the front-line choice of regimen in the treatment of patients with RCC, but responses may be modest or limited due to resistance of the tumor to anticarcinogen. Downregulated expression of organic cation transporter OCT2 is a possible mechanism underlying oxaliplatin resistance in RCC treatment. In this study, we observed that miR-489-3p and miR-630 suppress OCT2 expression by directly binding to the OCT2 3′-UTR. Meanwhile, via 786-O-OCT2-miRNAs stable expression cell models, we found that miRNAs could repress the classic substrate 1-methyl-4-phenylpyridinium (MPP+), fluorogenic substrate N,N-dimethyl-4-(2-pyridin-4-ylethenyl) aniline (ASP+), and oxaliplatin uptake by OCT2 both in vitro and in xenografts. In 33 clinical samples, miR-489-3p and miR-630 were significantly upregulated in RCC, negatively correlating with the OCT2 expression level compared to that in adjacent normal tissues, using tissue microarray analysis and qPCR validation. The increased binding of c-Myc to the promoter of pri-miR-630, responsible for the upregulation of miR-630 in RCC, was further evidenced by chromatin immunoprecipitation and dual-luciferase reporter assay. Overall, this study indicated that miR-489-3p and miR-630 function as oncotherapy-obstructing microRNAs by directly targeting OCT2 in RCC. KEY WORDS: OCT2, miRNA, Renal cell carcinoma, Epigenetic regulation, Oxaliplatin
Renal cell carcinoma (RCC) is one of the most common malignant tumors affecting the urogenital system, accounting for 90% of renal malignancies. Traditional chemotherapy options are often the front-line choice of regimen in the treatment of patients with RCC, but responses may be modest or limited due to resistance of the tumor to anticarcinogen. Downregulated expression of organic cation transporter OCT2 is a possible mechanism underlying oxaliplatin resistance in RCC treatment. In this study, we observed that miR-489-3p and miR-630 suppress OCT2 expression by directly binding to the OCT2 3′-UTR. Meanwhile, via 786-O-OCT2-miRNAs stable expression cell models, we found that miRNAs could repress the classic substrate 1-methyl-4-phenylpyridinium (MPP + ), fluorogenic substrate N , N -dimethyl-4-(2-pyridin-4-ylethenyl) aniline (ASP + ), and oxaliplatin uptake by OCT2 both in vitro and in xenografts. In 33 clinical samples, miR-489-3p and miR-630 were significantly upregulated in RCC, negatively correlating with the OCT2 expression level compared to that in adjacent normal tissues, using tissue microarray analysis and qPCR validation. The increased binding of c-Myc to the promoter of pri-miR-630, responsible for the upregulation of miR-630 in RCC, was further evidenced by chromatin immunoprecipitation and dual-luciferase reporter assay. Overall, this study indicated that miR-489-3p and miR-630 function as oncotherapy-obstructing microRNAs by directly targeting OCT2 in RCC. MiR-489-3p, c-Myc and miR-630 mediate OCT2 downregulation in RCC cells. MiR-489-3p and miR-630 is abnormally upregulated in RCC samples and exosomes, suppressing OCT2 expression by directly binding to the OCT2 3′-UTR. The increased binding of c-Myc to the promoter of pri-miR-630, contributes to the upregulation of miR-630 in RCC. fx1
Author Lei, Jinxiu
Zeng, Kui
Chen, Lu
Chen, Le
Qin, Zhiyuan
Ye, Sheng
Ying, Meidan
Yu, Lushan
Wang, Hua
Gao, Jianqing
Zeng, Su
AuthorAffiliation a Institute of Drug Metabolism and Pharmaceutical Analysis, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China
b Paediatric Intensive Care Unit, the Children׳s Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
c Department of Urology, Cancer Hospital of Zhejiang Province, Hangzhou 310022, China
AuthorAffiliation_xml – name: c Department of Urology, Cancer Hospital of Zhejiang Province, Hangzhou 310022, China
– name: b Paediatric Intensive Care Unit, the Children׳s Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
– name: a Institute of Drug Metabolism and Pharmaceutical Analysis, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China
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Snippet Renal cell carcinoma (RCC) is one of the most common malignant tumors affecting the urogenital system, accounting for 90% of renal malignancies. Traditional...
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Title Upregulation of miR-489-3p and miR-630 inhibits oxaliplatin uptake in renal cell carcinoma by targeting OCT2
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