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Related Concept Videos

Cancer02:18

Cancer

Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
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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Related Experiment Video

Updated: Jun 23, 2026

Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer
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Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer

Published on: July 18, 2017

Pericytes limit tumor cell metastasis.

Xiaojie Xian1, Joakim Håkansson, Anders Ståhlberg

  • 1Stem Cell Center, Lund University, Lund, Sweden.

The Journal of Clinical Investigation
|February 14, 2006
PubMed
Summary

Neural cell adhesion molecule (NCAM) deficiency in tumors promotes metastasis by disrupting blood vessel integrity and pericyte function. Restoring NCAM stabilizes vessels, reducing tumor spread and improving outcomes.

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Micromanipulation of Circulating Tumor Cells for Downstream Molecular Analysis and Metastatic Potential Assessment

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Area of Science:

  • Oncology
  • Cell Biology
  • Vascular Biology

Background:

  • Neural cell adhesion molecule (NCAM) deficiency in beta tumor cells was previously linked to increased metastasis.
  • Tumor microenvironment, particularly blood vessel stability, plays a crucial role in cancer progression.

Purpose of the Study:

  • To investigate the role of NCAM in regulating tumor metastasis.
  • To determine if pericyte dysfunction contributes to increased metastatic potential.

Main Methods:

  • Examined NCAM-deficient beta cell tumors for blood vessel integrity and pericyte interactions.
  • Assessed NCAM expression in a fibrosarcoma model (T241) for effects on pericyte recruitment and ECM deposition.
  • Studied beta cell tumorigenesis in pericyte-deficient Pdgfb(ret/ret) mice.

Main Results:

  • NCAM-deficient tumors exhibited leaky blood vessels with impaired pericyte-endothelial cell interactions and reduced ECM deposition.
  • Tumor cell NCAM expression enhanced pericyte recruitment and perivascular ECM deposition.
  • Pericyte deficiency led to beta tumor cell metastases, confirming their role in limiting tumor spread.

Conclusions:

  • NCAM stabilizes the microvessel wall, thereby limiting tumor cell metastasis.
  • Tumor cell metastasis is facilitated by the perturbation of pericyte-endothelial cell interactions.
  • Pericytes are critical in preventing tumor cell metastasis.