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Related Concept Videos

Enzyme-linked Receptors01:00

Enzyme-linked Receptors

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Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
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TNF receptor 2 knockout mouse had reduced lung cancer growth and schizophrenia-like behavior through a decrease in

In Jun Yeo1, Ji Eun Yu2, Sung-Hyun Kim3

  • 1College of Pharmacy, Kyungpook National University, 80 Daehak-ro, Buk-gu, Daegu, 41566, Republic of Korea.

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Tumor necrosis factor receptor 2 (TNFR2) plays a key role in both lung cancer growth and schizophrenia-like behaviors. Targeting TNFR2 may offer a novel therapeutic strategy for these comorbid conditions.

Keywords:
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Area of Science:

  • Neuroscience
  • Oncology
  • Immunology

Background:

  • The link between schizophrenia (SCZ) and cancer is debated.
  • Tumor necrosis factor receptor (TNFR) is implicated in both SCZ and cancer.
  • The specific role of TNFR in mediating SCZ and cancer comorbidity is unclear.

Purpose of the Study:

  • To investigate the role of TNFR2 in lung cancer progression and SCZ-like behaviors.
  • To elucidate the molecular mechanisms underlying the association between TNFR2, brain-derived neurotrophic factor (BDNF), and tropomyosin receptor kinase B (TrkB).

Main Methods:

  • Utilized TNFR2 knockout mice xenografted with A549 lung cancer cells.
  • Assessed tumor growth, SCZ-like behaviors, and expression levels of BDNF and TrkB.
  • Conducted in vitro studies using A549 cells with siTNFR2 transfection and BDNF treatment.

Main Results:

  • TNFR2 knockout mice exhibited reduced tumor size, weight, and SCZ-like behaviors.
  • TrkB and BDNF levels were decreased in tumors and brain tissue of TNFR2 knockout mice.
  • Exogenous BDNF administration restored tumor growth and SCZ-like behaviors in knockout mice, while BDNF addition rescued cell growth and TrkB expression in vitro.

Conclusions:

  • TNFR2 is a critical mediator in the comorbidity of lung tumor growth and SCZ development.
  • The TNFR2-dependent regulation of BDNF and TrkB signaling pathways is crucial for this association.