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Related Concept Videos

Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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...
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.
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Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...

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Related Experiment Video

Updated: May 14, 2026

A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer
07:35

A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer

Published on: December 26, 2016

Signaling Networks Regulating Metastatic Progression in Triple-Negative Breast Cancer.

Zuzanna Senkowska1, Katarzyna Owczarek1, Karolina Niewinna1

  • 1Department of Biochemistry, Faculty of Medicine, Medical University of Lodz, 92-215 Lodz, Poland.

Cells
|May 13, 2026
PubMed
Summary
This summary is machine-generated.

Triple-negative breast cancer (TNBC) is aggressive due to metastasis. Understanding key signaling pathways like PI3K/Akt and TGF-β is crucial for developing new treatments to combat TNBC spread.

Keywords:
cancer stem cellsepithelial–mesenchymal transitionmetastasissignaling pathwaystriple-negative breast cancertumor microenvironment

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Last Updated: May 14, 2026

A Portal Vein Injection Model to Study Liver Metastasis of Breast Cancer
07:35

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Published on: December 26, 2016

Modeling Brain Metastasis Via Tail-Vein Injection of Inflammatory Breast Cancer Cells
05:02

Modeling Brain Metastasis Via Tail-Vein Injection of Inflammatory Breast Cancer Cells

Published on: February 4, 2021

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype lacking ER, PR, and HER2 expression.
  • Limited therapeutic options and high metastatic potential contribute to TNBC mortality.
  • Metastasis in TNBC is driven by complex, interconnected molecular signaling networks.

Purpose of the Study:

  • To review molecular mechanisms of TNBC metastatic progression.
  • To emphasize signaling pathways regulating invasion, migration, and distant organ colonization.
  • To identify potential therapeutic targets for limiting TNBC metastasis.

Main Methods:

  • Literature review of current knowledge on TNBC metastasis.
  • Focus on key signaling pathways: PI3K/Akt, TGF-β, Wnt/β-catenin, NF-κB, Rho/ROCK.
  • Discussion of pathway roles in epithelial-mesenchymal transition, cytoskeletal remodeling, CSC phenotypes, and TME interactions.

Main Results:

  • Identified PI3K/Akt, TGF-β, Wnt/β-catenin, NF-κB, and Rho/ROCK as key regulators of TNBC metastasis.
  • Highlighted their roles in epithelial-mesenchymal transition, cell migration, and invasion.
  • Emphasized the importance of tumor-microenvironment interactions in metastatic progression.

Conclusions:

  • Deeper understanding of these signaling networks is essential for TNBC research.
  • These pathways represent potential targets for novel therapeutic strategies.
  • Effective strategies are needed to limit metastatic disease and improve outcomes for TNBC patients.