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

LncRNA FALEC通过竞争性调控miR-20a-5p/SHOC2轴促进胆管癌增殖、迁移和耐药

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作者:Haiming Du, Senlin Hou, Lichao Zhang, Chao Liu, Tingting Yu, Wei Zhang

Background

LncRNA is an important regulatory factor in the human genome. We

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.

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.

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