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Research Paper|Volume 11, Issue 20|pp 8860—8878

Long non-coding SBF2-AS1 acting as a competing endogenous RNA to sponge microRNA-142-3p to participate in gemcitabine resistance in pancreatic cancer via upregulating TWF1

Yong-Qiang Hua1,2, Yao-Dong Zhu3, Guo-Qun Xie4, Ke Zhang1,2, Jie Sheng1,2, Zhen-Feng Zhu1,2, Zhou-Yu Ning1,2, Hao Chen1,2, Zhen Chen1,2, Zhi-Qiang Meng1,2, Lu-Ming Liu1,2
  • 1Minimally Invasive Treatment Center, Fudan University Shanghai Cancer Center, Shanghai 200032, PR China
  • 2Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, PR China
  • 3Chinese Integrative Medicine Oncology Department, First Affiliated Hospital of Medical University of Anhui, Hefei 230000, Anhui Province, PR China
  • 4Oncology Department, Yueyang Hospital of Integrative Chinese and Western Medicine Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200437, PR China
Received: May 24, 2019Accepted: September 17, 2019Published: October 16, 2019
https://doi.org/10.18632/aging.102307

Copyright © 2019 Hua et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Objective: This study is implemented to probe into the function of lncRNA SBF2-AS1 as a competing endogenous RNA (ceRNA) to sponge microRNA-142-3p (miR-142-3p) in modulating TWF1 expression in the gemcitabine resistance of pancreatic cancer.

Results: LncRNA SBF2-AS1 was highly expressed in pancreatic cancer tissues and cells. SBF2-AS1 was found to be associated with gemcitabine resistance in pancreatic cancer. Knock-down of SBF2-AS1 inhibited proliferation, epithelial-mesenchymal transition, while promoting apoptosis of gemcitabine resistant pancreatic cancer cells. SBF2-AS1 inhibited the expression of TWF1 by competitively binding with miR-142-3p in pancreatic cancer.

Conclusion: Our study demonstrates that knock-down of SBF2-AS1 inhibits the expression of TWF1 by competitively binding with miR-142-3p to induce gemcitabine resistance in pancreatic cancer.

Methods: Expression of SBF2-AS1 was tested in pancreatic cancer tissues and cells. Construction of AsPC-1/GEM and PANC-1/GEM cells with low expression of SBF2-AS1 was performed to determine the biological behaviors of drug-resistant cells. AsPC-1 and PANC-1 cells expressing SBF2-AS1 and/or miR-142-3p were constructed and treated with different concentrations of gemcitabine to detect the sensitivity of the cells to gemcitabine. The binding relationship between SBF2-AS1 and miR-142-3p and between miR-142-3p and TWF1 were determined.