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MBIP (MAP3K12 binding inhibitory protein) drives NSCLC metastasis by JNK-dependent activation of MMPs

Joshua Kapere Ochieng1, Samrat T Kundu2, Rakhee Bajaj1

  • 1Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX, 77030, USA.

Oncogene
|September 23, 2020
PubMed

Insights

MBIP (MAP3K12 binding inhibitory protein) drives non-small cell lung cancer (NSCLC) progression. This protein enhances tumor cell invasion and metastasis by activating the JNK pathway and matrix metalloproteinases (MMPs).

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Metastasis is responsible for 90% of cancer mortality.
  • Identifying genetic drivers of tumor cell dissemination is crucial for developing new therapies.
  • Previous research identified ~30 genes promoting metastasis, including MBIP.

Purpose of the Study:

  • To investigate the role of MBIP (MAP3K12 binding inhibitory protein) in driving tumor invasion and metastasis.
  • To elucidate the molecular mechanisms by which MBIP promotes non-small cell lung cancer (NSCLC) progression.

Main Methods:

  • In vitro assays assessing cellular proliferation, migration, and invasion of NSCLC cells.
  • In vivo metastasis models to evaluate MBIP's effect on tumor dissemination.
  • Analysis of MBIP's impact on JNK pathway activation and matrix metalloproteinase (MMP) expression.

Main Results:

  • MBIP expression significantly enhanced NSCLC cell proliferation, migration, and invasion in vitro.
  • MBIP expression led to increased metastasis in vivo.
  • MBIP was found to activate the JNK pathway and induce MMP expression, crucial for invasion and metastasis.

Conclusions:

  • MBIP acts as a novel driver of NSCLC progression and metastasis.
  • MBIP promotes cancer cell invasiveness through JNK pathway activation and MMP induction.
  • Targeting MBIP may offer a therapeutic strategy for combating NSCLC metastasis.

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