Related Experiment Video

Updated: Dec 13, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

14.0K

TrkB Inhibits the BMP Signaling-Mediated Growth Inhibition of Cancer Cells

Min Soo Kim1, Wook Jin1

  • 1Laboratory of Molecular Disease and Cell Regulation, Department of Biochemistry, School of Medicine, Gachon University, Incheon 21999, Korea.

Cancers
|August 1, 2020
PubMed

Insights

Tropomyosin receptor kinase B (TrkB) promotes breast cancer metastasis by suppressing bone morphogenetic protein (BMP) signaling. Inhibiting TrkB restores BMP-2

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Tropomyosin receptor kinase B (TrkB) is implicated in breast cancer metastasis.
  • TrkB activates JAK2/STAT3 and PI3K/AKT pathways, inhibiting RUNX3 and KEAP1.
  • The role of TrkB in regulating bone morphogenetic protein (BMP) signaling and tumor suppression is largely unknown.

Purpose of the Study:

  • To investigate the role of TrkB in regulating BMP signaling and tumor suppression in breast cancer.
  • To elucidate the mechanisms by which TrkB influences BMP-mediated tumor suppression.

Main Methods:

  • Cell culture and manipulation (TrkB knockdown).
  • Analysis of cell proliferation, anchorage-independent growth, and migration.
  • Western blotting and co-immunoprecipitation to study protein interactions and signaling pathways (BMP, SMAD1, RUNX3).
  • Assessment of TrkB kinase activity.

Main Results:

  • TrkB enhances breast cancer cell anchorage-independent growth and migration.
  • TrkB suppresses BMP-2-mediated growth inhibition.
  • TrkB inhibits BMP-mediated SMAD1 activation by forming a complex with the BMP type II receptor.
  • TrkB suppresses RUNX3 expression by depleting BMP receptor I.
  • TrkB knockdown restores BMP-2's tumor-inhibitory effect via SMAD1 activation.
  • TrkB kinase activity is essential for its effects on BMP signaling.

Conclusions:

  • TrkB is a key regulator of BMP-mediated tumor suppression in breast cancer.
  • TrkB interferes with BMP signaling pathways, promoting cancer cell proliferation and metastasis.
  • Targeting TrkB may represent a therapeutic strategy to restore BMP-mediated tumor suppression.
Keywords:
BMP type I (BMPRI) and BMP type II (BMPRII) receptorTrkBbone morphogenetic proteins (BMPs)tumor progressiontumor suppressor activity

More Related Videos

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

18.4K
Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion09:23

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion

Published on: April 2, 2020

6.8K

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.5K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.4K
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

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...
84.7K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.0K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.5K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.0K