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L290P/V mutations increase ERK3's cytoplasmic localization and migration/invasion-promoting capability in cancer

Hadel Alsaran1, Lobna Elkhadragy1, Astha Shakya1

  • 1Department of Biochemistry and Molecular Biology, Boonshoft School of Medicine, Wright State University, Dayton, Ohio, USA.

Scientific Reports
|November 5, 2017
PubMed

Insights

Mutations in ERK3 (a protein kinase) enhance cancer cell invasion and migration. These L290P/V mutations increase cytoplasmic localization, potentially driving cancer metastasis in lung and colon cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Protein kinases are crucial in cancer signaling pathways.
  • ERK3, an atypical mitogen-activated protein kinase (MAPK), plays a role in cancer progression, migration, and metastasis.
  • ERK3 mutations are not well understood in cancer contexts.

Purpose of the Study:

  • To functionally and mechanistically characterize ERK3 L290P/V mutations found in human cancers.
  • To investigate the impact of these mutations on cancer cell behavior and signaling.

Main Methods:

  • Site-directed mutagenesis to create L290P and L290V ERK3 variants.
  • In vitro assays measuring cancer cell migration and invasion.
  • Analysis of ERK3 protein localization and interaction with CRM1.

Main Results:

  • ERK3 L290P/V mutants showed significantly increased cancer cell migration and invasion compared to wild-type ERK3.
  • These mutations had minimal effect on ERK3's role in cell proliferation.
  • Mutations enhanced cytoplasmic localization of ERK3 by increasing interaction with the nuclear export factor CRM1, without altering kinase activity.

Conclusions:

  • ERK3 L290P/V mutations may enhance cancer invasiveness.
  • These findings highlight a novel mechanism by which ERK3 mutations contribute to cancer progression and metastasis.

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