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Related Concept Videos

Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...
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Cell Migration

Cell migration is a process by which the cells move from one location to another, playing an essential role in embryological development, repair and regeneration, immune response, and metastasis. Cells migrate in response to chemical or mechanical signals generated by specific organs or tissues. The overall mechanism includes three steps - polarization, protrusion, and release. Polarization involves the formation of a distinct cell front and rear, which determines the direction of movement.
Cell Migration01:09

Cell Migration

Cell migration, the process by which cells move from one location to another, is essential for the proper development and viability of organisms throughout their life. When cells are not able to migrate properly to their ordained locations, various disorders may occur. For example, disruption in cell migration causes chronic inflammatory diseases such as arthritis.
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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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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Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies
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Overexpression of forkhead box J2 can decrease the migration of breast cancer cells.

Yingying Wang1, Shuyun Yang, Qichao Ni

  • 1Department of Immunology, Medical College, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.

Journal of Cellular Biochemistry
|March 24, 2012
PubMed
Summary
This summary is machine-generated.

Forkhead Box J2 (FOXJ2) inhibits breast cancer metastasis by regulating epithelial-mesenchymal transition (EMT) markers. Higher FOXJ2 expression correlates with reduced metastasis, suggesting its potential as a therapeutic target.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Breast cancer metastasis significantly worsens patient prognosis, necessitating research into underlying molecular mechanisms.
  • Forkhead Box J2 (FOXJ2), a transcription factor, is implicated in tumor cell migration and invasion.
  • Understanding FOXJ2's role is crucial for developing novel therapeutic strategies against metastatic breast cancer.

Purpose of the Study:

  • To investigate the novel function of Forkhead Box J2 (FOXJ2) in breast cancer metastasis.
  • To elucidate the molecular mechanisms by which FOXJ2 influences cancer cell motility and epithelial-mesenchymal transition (EMT).

Main Methods:

  • Analysis of FOXJ2 expression in primary breast cancer tissues with and without lymph node metastasis.
  • In vitro assays (wound healing, trans-well migration) to assess cell motility upon FOXJ2 modulation.
  • Western blot, RT-PCR, and immunofluorescence to evaluate EMT markers (E-cadherin, vimentin) and FOXJ2 expression.

Main Results:

  • FOXJ2 expression was significantly higher in breast cancer tissues lacking lymph node metastasis.
  • Overexpression of FOXJ2 reduced the motility of highly metastatic MDA-MB-231 cells.
  • Repression of FOXJ2 enhanced the motility of weakly metastatic MCF-7 cells, accompanied by altered E-cadherin and vimentin expression.

Conclusions:

  • FOXJ2 acts as a suppressor of breast cancer metastasis.
  • FOXJ2 inhibits metastasis by regulating epithelial-mesenchymal transition (EMT) key markers, E-cadherin and vimentin.
  • These findings highlight FOXJ2 as a potential therapeutic target for preventing breast cancer spread.