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Research Paper|Volume 15, Issue 9|pp 3759—3770

LncRNA FALEC increases the proliferation, migration and drug resistance of cholangiocarcinoma through competitive regulation of miR-20a-5p/SHOC2 axis

Haiming Du1, Senlin Hou1, Lichao Zhang1, Chao Liu2, Tingting Yu1, Wei Zhang1
  • 1The Biliopancreatic Endoscopic Surgery Department, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei Province, China
  • 2Department of Anesthesiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei Province, China
Received: February 15, 2023Accepted: April 17, 2023Published: May 9, 2023
https://doi.org/10.18632/aging.204709

Copyright: © 2023 Du 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

Background: LncRNA is an important regulatory factor in the human genome. We aim to explore the roles of LncFALEC and miR-20a-5p/SHOC2 axis on the proliferation, migration, and Fluorouracil (5-FU) resistance of cholangiocarcinoma (CCA).

Methods: In this study, the expression of FALEC and miR-20a-5p in CCA tissues and cell lines (HuCCT1, QBC939, and Huh-28) was detected by RT-qPCR. The FALEC in 5-FU-resistant CCA cell lines (QBC939-R, Huh-28-R) was knocked down to evaluate its effects on cell proliferation, migration, invasion, and drug resistance.

Results: Our analysis showed that compared with the adjacent non-tumor tissues, FALEC was significantly higher in the CCA tissues and even higher in the samples from 5-FU-resistant patients. Knockdown FALEC increased the sensitivity of 5-FU and decreased migration and invasion of CCA cells. Dual luciferase reporter confirmed that FALEC sponges miR-20a-5p and down-regulated its expression. Moreover, SHOC2 leucine-rich repeat scaffold protein (SHOC2) was the target gene of miR-20a-5p. We found overexpression of FALEC (FALEC-OE) increased resistance of CCA cells to 5-FU significantly, which might contribute to increased SHOC2 expression and activation of the ERK1/2 signaling pathway.

Conclusions: In summary, our study revealed that down-regulation of FALEC could inhibit the proliferation, migration, and invasion of CCA cells in vitro by regulating the miR-20a-5p/SHOC2 axis and participating in 5-FU resistance by mediating the ERK1/2 signaling pathway.