MiR-16-1 Targeted Silences Far Upstream Element Binding Protein 1 to Advance the Chemosensitivity to Adriamycin in Gastric Cancer

MiR-16-1 Targeted Silences Far Upstream Element Binding Protein 1 to Advance the Chemosensitivity... Chemotherapy can prevent metastasis and recurrence of gastric cancer (GC), and is a well supplement for operation. But, chemotherapy resistance has severely restricted the application of chemotherapy. This study aimed to investigate the regulatory roles and molecular mechanism of miR-16-1 to the chemosensitivity to adriamycin in GC. In this study, the expression of miR-16-1 and FUBP1 was down-regulated and up-regulated respectively in adriamycin-resistant GC tissues and cell lines, and represented a negative relationship between them. MiR-16-1 could silence FUBP1 directly and specifically, FUBP1 was a target gene of miR-16-1. Silence of FUBP1 inhibited the half maximal inhibitory concentration (IC50) of SGC7901/AR cell line to adriamycin, chemosensitivity enhanced significantly. Moreover, FUBP1 silence in SGC7901/AR cell line also inhibited proliferation and invasion, and advanced cell apoptosis. To sum up, the expression of miR-16-1 was positively related with the chemosensitivity of GC to adriamycin, and miR-16-1 could targeted silence FUBP1 to advance the chemosensitivity to adriamycin in GC, which might be a novel potential therapeutic target for GC. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Pathology & Oncology Research Springer Journals

MiR-16-1 Targeted Silences Far Upstream Element Binding Protein 1 to Advance the Chemosensitivity to Adriamycin in Gastric Cancer

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Publisher
Springer Netherlands
Copyright
Copyright © 2017 by Arányi Lajos Foundation
Subject
Biomedicine; Cancer Research; Oncology; Pathology; Immunology; Biomedicine, general
ISSN
1219-4956
eISSN
1532-2807
D.O.I.
10.1007/s12253-017-0263-x
Publisher site
See Article on Publisher Site

Abstract

Chemotherapy can prevent metastasis and recurrence of gastric cancer (GC), and is a well supplement for operation. But, chemotherapy resistance has severely restricted the application of chemotherapy. This study aimed to investigate the regulatory roles and molecular mechanism of miR-16-1 to the chemosensitivity to adriamycin in GC. In this study, the expression of miR-16-1 and FUBP1 was down-regulated and up-regulated respectively in adriamycin-resistant GC tissues and cell lines, and represented a negative relationship between them. MiR-16-1 could silence FUBP1 directly and specifically, FUBP1 was a target gene of miR-16-1. Silence of FUBP1 inhibited the half maximal inhibitory concentration (IC50) of SGC7901/AR cell line to adriamycin, chemosensitivity enhanced significantly. Moreover, FUBP1 silence in SGC7901/AR cell line also inhibited proliferation and invasion, and advanced cell apoptosis. To sum up, the expression of miR-16-1 was positively related with the chemosensitivity of GC to adriamycin, and miR-16-1 could targeted silence FUBP1 to advance the chemosensitivity to adriamycin in GC, which might be a novel potential therapeutic target for GC.

Journal

Pathology & Oncology ResearchSpringer Journals

Published: Jun 30, 2017

References

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