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KSRP modulates melanoma growth and efficacy of vemurafenib

Wenwen Liu1, Chu-Fang Chou2, Shanrun Liu3

  • 1State Key Laboratory of Structured Chemistry, Fujian Institute of Research on the Structure of Matter, Chinese Academy of Sciences, Fuzhou, Fujian 350002, China; University of Chinese Academy of Sciences, Beijing 100049, China; Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, United States of America.

Biochimica Et Biophysica Acta. Gene Regulatory Mechanisms
|July 4, 2019
PubMed

Insights

KH-type splicing regulatory protein (KSRP) drives melanoma cell proliferation and vemurafenib resistance. Silencing KSRP reduces melanoma growth by increasing killin (KLLN) mRNA decay, offering new therapeutic targets for advanced melanoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Most melanomas harbor BRAFV600E mutations, driving proliferation.
  • BRAF inhibitors (BRAFi) induce tumor shrinkage but acquired resistance is common.
  • Identifying melanoma growth regulators and resistance factors is key for better therapies.

Purpose of the Study:

  • To investigate the role of KH-type splicing regulatory protein (KSRP) in melanoma proliferation.
  • To determine KSRP's involvement in acquired resistance to BRAFi.
  • To identify downstream effectors of KSRP in melanoma.

Main Methods:

  • KSRP silencing in melanoma cell lines.
  • Assessment of cell proliferation and response to vemurafenib.
  • Analysis of killin (KLLN) mRNA levels and stability.
  • RNA-protein interaction studies and mRNA reporter assays.

Main Results:

  • KSRP is crucial for melanoma cell proliferation, both with and without vemurafenib resistance.
  • KSRP silencing reduces proliferation and enhances vemurafenib's growth-suppressive effects.
  • KSRP promotes KLLN mRNA decay via interaction with a U-rich element in the 3' UTR.
  • KLLN, a p53-regulated DNA replication inhibitor, is a downstream effector of KSRP silencing.

Conclusions:

  • KSRP is a critical regulator of melanoma cell growth.
  • KSRP influences melanoma progression and BRAFi resistance partly by controlling KLLN mRNA stability.
  • Targeting KSRP may offer a strategy for durable responses in advanced melanoma.
Keywords:
KSRPMelanomaRNA-binding proteinVemurafenibmRNA decay

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