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Related Concept Videos

Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

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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,...
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Metastasis

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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.
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Endocytosis01:16

Endocytosis

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Eukaryotic cells acquire nutrients for growth and proliferation. Nutrients and other molecules that require degradation are internalized from the extracellular space by a process called endocytosis. The term ‘endocytosis' was first coined by Christian de Duve in 1963.
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Adaptive Mechanisms in Cancer Cells02:53

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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.
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Adaptive Mechanisms in Cancer Cells

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Receptor-mediated Endocytosis01:20

Receptor-mediated Endocytosis

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Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
Clathrin-Mediated Endocytosis of LDL
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Related Experiment Video

Updated: May 5, 2026

Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes
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Endocytosis and cancer.

Ira Mellman1, Yosef Yarden

  • 1Genentech Inc., South San Francisco, California 94080.

Cold Spring Harbor Perspectives in Biology
|December 4, 2013
PubMed
Summary

Cancer cells hijack endocytosis to promote tumor growth by altering cell surface protein recycling. Targeting these altered pathways offers new therapeutic strategies for cancer treatment.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Endocytosis is crucial for regulating cell-surface proteins, involving sorting events for degradation or recycling.
  • This process relies on sequence motifs, posttranslational modifications, and protein assemblies.
  • Cancer cells exhibit altered endocytosis, impacting tumor progression.

Purpose of the Study:

  • To review how cancer drivers like p53 and Ras influence endocytosis.
  • To examine the role of altered endocytosis in cancer cell motility and tissue disruption.
  • To discuss pharmacological strategies targeting cancer's endocytic system.

Main Methods:

  • Literature review of endocytosis mechanisms in cancer.
  • Analysis of protein sorting, recycling, and degradation pathways.

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Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics
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Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics

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Fluorescence Microscopy for ATP Internalization Mediated by Macropinocytosis in Human Tumor Cells and Tumor-xenografted Mice
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Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics
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  • Examination of the roles of p53, Ras, integrins, RTKs, and cadherins in cancer endocytosis.

    • Main Results:

    • p53 and Ras bias recycling of integrins and receptor tyrosine kinases (RTKs) in cancer cells.
    • Cadherins and junctional proteins are removed from cancer cell surfaces, promoting motility.
    • Mutant RTKs evading ubiquitination and defective feedback loops are common in tumors.

    Conclusions:

    • Cancer cells exploit endocytosis for growth and metastasis.
    • Targeting aberrant endocytic pathways presents a promising therapeutic avenue for cancer treatment.