Splicing factor RBM10 loss fuels thyroid cancer metastasis

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Updated: May 26, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

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Kevin Coughlin1, Ledong Wan1,2

  • 1Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, NY, USA.

The Journal of Experimental Medicine
|February 24, 2025
PubMed

Insights

Loss of the splicing factor RBM10 drives thyroid cancer metastasis by altering RNA splicing. This discovery reveals a potential therapeutic vulnerability linked to NF-κB signaling.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Thyroid cancer metastasis remains a significant clinical challenge.
  • The role of RNA splicing regulation in cancer progression is increasingly recognized.

Purpose of the Study:

  • To investigate the role of the splicing factor RBM10 in thyroid cancer metastasis.
  • To identify potential therapeutic targets based on molecular alterations in thyroid cancer.

Main Methods:

  • Analysis of RNA splicing patterns in thyroid cancer.
  • Investigating the functional impact of RBM10 loss in cancer cells.
  • Exploring synthetic lethal interactions involving RBM10 and NF-κB pathways.

Main Results:

  • Loss of RBM10 was identified as a key driver of thyroid cancer metastasis.
  • RBM10 regulates metastasis through the modulation of RNA splicing.
  • A synthetic lethal interaction between NF-κB and RBM10 loss was uncovered.

Conclusions:

  • RBM10 is a critical regulator of RNA splicing and a driver of thyroid cancer metastasis.
  • Targeting the interplay between NF-κB and RBM10 loss presents a promising therapeutic strategy for thyroid cancer.

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