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Title: Long non-coding RNA KCNQ1OT1 modulates oxaliplatin resistance in hepatocellular carcinoma through miR-7-5p/ ABCC1 axis

Journal Article · · Biochemical and Biophysical Research Communications
;  [1];  [2];  [3]
  1. Department of Chinese Medicine, Affiliated Longhua Central Hospital, Guangdong Medical University, Shenzhen, 518110, Guangdong (China)
  2. Department of Quality Control, Affiliated Longhua Central Hospital, Guangdong Medical University, Shenzhen, 518110, Guangdong (China)
  3. Department of Medical Laboratory, Affiliated Longhua Central Hospital, Guangdong Medical University, Shenzhen, 518110, Guangdong (China)

Highlights: • KCNQ1OT1 was significantly up-regulated in oxaliplatin-resistant HCC cells. • Knockdown of KCNQ1OT1 inhibited the cell proliferation, migration, invasion. • KCNQ1OT1 modulated oxaliplatin resistance in HCC through miR-7-5p/ ABCC1 axis. The underlying functions of long non-coding RNAs (lncRNAs) on chemoresistance in multiple cancers have been testified. However, the function and mechanism of lncRNAs on chemoresistance in hepatocellular carcinoma are still confused. In this study, we concentrated on the function and mechanism of KCNQ1OT1 on oxaliplatin resistance in hepatocellular carcinoma. Results showed that KCNQ1OT1 was significantly up-regulated in oxaliplatin-resistant HepG2 and Huh7 cells. Moreover, knockdown of KCNQ1OT1 inhibited the cell proliferation, migration, invasion and reduced the expression of drug-resistant gene (MRP5, MDR1, LRP1). Additionally, bioinformatics analysis and dual-luciferase reporter assay showed that miR-7-5p directly targeted the 3′-UTR of miR-7-5p and ABCC1 mRNA, indicating that KCNQ1OT1 regulated the expression of ABCC1 via endogenous sponging miR-7-5p. Conclusively, KCNQ1OT1 modulated oxaliplatin resistance in hepatocellular carcinoma through miR-7-5p/ABCC1 axis, indicating a novel approach for the treatment of hepatocellular carcinoma.

OSTI ID:
23103646
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 503, Issue 4; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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