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Related Experiment Video

Updated: Jun 25, 2025

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
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MerTK Drives Proliferation and Metastatic Potential in Triple-Negative Breast Cancer.

Mari Iida1, Bridget E Crossman1, Kourtney L Kostecki1

  • 1Department of Human Oncology, University of Wisconsin-Madison, Madison, WI 53705, USA.

International Journal of Molecular Sciences
|May 25, 2024
PubMed
Summary

MerTK receptor tyrosine kinase drives triple-negative breast cancer (TNBC) growth and metastasis, partly by increasing endoglin (ENG) expression. Simultaneous targeting of MerTK and ENG may offer new therapeutic strategies for TNBC.

Keywords:
MerTKTNBCendoglinlung metastases

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) lacks targeted therapies due to absent estrogen receptor, progesterone receptor, and HER2 expression.
  • Understanding TNBC molecular drivers is crucial for developing novel combinatorial treatments.
  • The role of MerTK receptor tyrosine kinase in TNBC proliferation and metastasis requires further investigation.

Purpose of the Study:

  • To evaluate the role of MerTK in TNBC proliferation and invasion/metastatic potential.
  • To investigate the downstream signaling pathways and molecular effectors regulated by MerTK in TNBC.
  • To determine if endoglin (ENG) mediates MerTK's pro-metastatic effects in TNBC.

Main Methods:

  • Immunohistochemistry to assess MerTK expression in patient-derived TNBC xenografts.
  • Stable overexpression of MerTK in human TNBC cell lines (SUM102).
  • NanoString nCounter analysis and proteomic profiling to identify MerTK-regulated pathways and proteins.
  • CRISPR-Cas9 technology to knock out endoglin (ENG) in MerTK-overexpressing TNBC cells.

Main Results:

  • MerTK was expressed in 58% of TNBC xenografts.
  • MerTK overexpression increased TNBC cell proliferation, in vivo tumor growth, migration, invasion, and lung metastasis.
  • MerTK signaling upregulated pathways promoting cell cycle progression and survival, and increased endoglin (ENG) production.
  • ENG knockout in MerTK-overexpressing cells significantly reduced lung metastasis (~4-fold) while maintaining tumor growth.

Conclusions:

  • MerTK promotes TNBC proliferation and metastasis, partly through upregulation of endoglin (ENG).
  • MerTK regulates a distinct proliferative signature in TNBC.
  • Simultaneous targeting of MerTK and ENG presents a potential novel therapeutic strategy for TNBC.