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miR-126-3p contributes to sorafenib resistance in hepatocellular carcinoma via downregulating SPRED1

Wenliang Tan1,2, Zhirong Lin1,2, Xianqing Chen3

  • 1Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.

Annals of Translational Medicine
|February 8, 2021
PubMed
Abstract

Insights

This study reveals that high miR-126-3p expression promotes sorafenib resistance in hepatocellular carcinoma (HCC) by downregulating SPRED1. Inhibiting miR-126-3p enhances sorafenib

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Sorafenib is a key treatment for advanced hepatocellular carcinoma (HCC).
  • Drug resistance to sorafenib significantly limits its therapeutic efficacy in HCC patients.
  • Understanding the molecular mechanisms of sorafenib resistance is crucial for improving treatment outcomes.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying sorafenib resistance in HCC.
  • To explore the role of microRNAs (miRNAs) in mediating sorafenib resistance.
  • To identify potential therapeutic targets for overcoming sorafenib resistance.

Main Methods:

  • Bioinformatic analysis of differentially expressed miRNAs in HCC.
  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to measure miR-126-3p and SPRED1 expression.
  • Cell viability, proliferation, migration, and invasion assays (CCK-8, EdU, clone formation, Transwell).
  • Dual-luciferase reporter assay and Western blotting to confirm target interaction.
  • In vivo anti-tumor efficacy evaluation in subcutaneous tumor models.

Main Results:

  • High expression of miR-126-3p correlated with increased sorafenib resistance in HCC cells.
  • miR-126-3p was identified as a direct regulator of SPRED1 expression.
  • Upregulation of SPRED1 enhanced HCC cell sensitivity to sorafenib.
  • miR-126-3p promoted sorafenib resistance by downregulating SPRED1 and activating the ERK signaling pathway.
  • Inhibition of miR-126-3p potentiated the anti-tumor effect of sorafenib in vivo.

Conclusions:

  • The miR-126-3p/SPRED1 axis plays a critical role in sorafenib resistance in HCC.
  • Targeting the miR-126-3p/SPRED1 pathway represents a potential therapeutic strategy.
  • Modulating miR-126-3p offers a promising approach to enhance sorafenib efficacy in HCC treatment.
Keywords:
ERK signaling pathwayhepatocellular carcinoma (HCC)miR-126-3psorafenib resistancesprouty-related EVH1 domain-containing protein 1 (SPRED1)

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