Related Experiment Video

Updated: Jan 11, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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STK38 Kinase Promotes Cell Migration Induced by Oncogenic Ras via MerTK Activation

Satoshi Ohta1, Kenji Tago2, Katsumi Kasashima1

  • 1Division of Structural Biochemistry, Department of Biochemistry, Jichi Medical University, Shimotsuke 329-0498, Tochigi, Japan.

International Journal of Molecular Sciences
|November 13, 2025
PubMed

Insights

Oncogenic Ras promotes cancer cell migration by upregulating the receptor tyrosine kinase MerTK. This study identifies STK38 as a key kinase in this pathway, offering new therapeutic targets for Ras-mutated cancers.

Area of Science:

  • Molecular oncology
  • Cell signaling pathways

Background:

  • Ras gene mutations are common in various cancers, yet effective treatments remain limited.
  • Oncogenic Ras signaling drives cancer progression through downstream effectors, necessitating identification of novel therapeutic targets.

Purpose of the Study:

  • To identify novel downstream effectors of oncogenic Ras signaling involved in cancer cell migration.
  • To elucidate the role of the serine/threonine kinase STK38 in Ras-induced cell migration.

Main Methods:

  • Purification of the MerTK complex from Ras-transformed NIH-3T3 cells.
  • Mass spectrometric analysis to identify binding partners of MerTK.
  • Knockdown studies of MerTK and STK38 to assess their impact on cell migration and signaling pathways.
  • Assessment of kinase activity and downstream effector activation (Rac1, Cdc42).

Main Results:

  • STK38 was identified as a MerTK binding partner in Ras-transformed cells.
  • Knockdown of STK38 or MerTK significantly attenuated H-Ras (G12V)-induced NIH-3T3 cell migration.
  • STK38 kinase activity was essential for Ras-induced cell migration and MerTK phosphorylation.
  • STK38 and MerTK are involved in the activation of Rac1 and Cdc42.

Conclusions:

  • STK38 plays a critical role in oncogenic Ras-induced cell migration, acting downstream of Ras and interacting with MerTK.
  • The MerTK-STK38 axis represents a potential therapeutic target for cancers with Ras mutations.
Keywords:
MerTKRasSTK38cell migration

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