Related Experiment Video

Updated: May 23, 2025

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells
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Long Noncoding RNA E2F1 Messenger RNA Stabilizing Factor (EMS) Promotes Sorafenib Resistance in Renal Cell Carcinoma

Pinxiao Wang1, Qian Deng2, Siyuan Pan3

  • 1Department of Urology, Xi'an Daxing Hospital Affiliated to Yan'an University, Xi'an, Shaanxi, China.

Journal of Biochemical and Molecular Toxicology
|March 11, 2025
PubMed

Insights

A new study reveals that the long noncoding RNA EMS is elevated in sorafenib-resistant kidney cancer. Targeting this RNA and its pathway can restore drug sensitivity, offering hope for treating resistant renal cell carcinoma (RCC).

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Renal cell carcinoma (RCC) is a deadly kidney cancer.
  • Sorafenib is a key treatment, but resistance is a major challenge.
  • Understanding resistance mechanisms is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the role of long noncoding RNA E2F1 messenger RNA stabilizing factor (EMS) in sorafenib resistance in RCC.
  • To identify molecular targets for overcoming sorafenib resistance in RCC.
  • To explore the lncRNA EMS/miR-363-3p/DUSP10 axis in RCC drug resistance.

Main Methods:

  • Analysis of lncRNA EMS expression in sorafenib-sensitive and resistant RCC tissues and cell lines.
  • Knockdown of lncRNA EMS in resistant RCC cells and assessment of sorafenib sensitivity.
  • In vivo studies using xenograft models to evaluate the therapeutic potential of lncRNA EMS silencing.
  • Investigation of the interaction between lncRNA EMS, miR-363-3p, and DUSP10.

Main Results:

  • lncRNA EMS expression was significantly higher in sorafenib-resistant RCC.
  • lncRNA EMS knockdown resensitized RCC cells to sorafenib, decreasing proliferation and increasing apoptosis.
  • Combined treatment of lncRNA EMS silencing and sorafenib inhibited tumor growth in vivo.
  • lncRNA EMS sponged miR-363-3p, leading to decreased miR-363-3p and increased DUSP10 expression, promoting sorafenib resistance.

Conclusions:

  • The lncRNA EMS/miR-363-3p/DUSP10 axis is a key regulator of sorafenib resistance in RCC.
  • lncRNA EMS acts as a molecular sponge for miR-363-3p, upregulating DUSP10 and conferring resistance.
  • These molecules represent potential therapeutic targets and biomarkers for sorafenib-resistant RCC.
Keywords:
DUSP10lncRNA EMSmiR‐363‐3prenal cell carcinomasorafenib resistance

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