Related Experiment Video
Updated: Nov 12, 2025
Automated Imaging and Analysis for the Quantification of Fluorescently Labeled Macropinosomes
Published on: August 24, 2021
Derailed endocytosis: an emerging feature of cancer
Yaron Mosesson1, Gordon B Mills, Yosef Yarden
1Department of Biological Regulation, The Weizmann Institute of Science, Rehovot 76100, Israel.
Abstract:
Once engaged by soluble or matrix-anchored ligands, cell surface proteins are commonly sorted to lysosomal degradation through several endocytic pathways. Defective vesicular trafficking of growth factor receptors, as well as unbalanced recycling of integrin- and cadherin-based adhesion complexes, has emerged in the past 5 years as a multifaceted hallmark of malignant cells. In line with the cooperative nature of endocytic machineries, multiple oncogenic alterations underlie defective endocytosis, such as altered ubiquitylation (Cbl and Nedd4 ubiquitin ligases, for example), altered cytoskeletal interactions and alterations to Rab family members. Pharmaceutical interception of the propensity of tumour cells to derail their signalling and their adhesion receptors may constitute a novel target for cancer therapy.
Insights
Cancer cells hijack endocytic pathways to degrade cell surface proteins, disrupting signaling and adhesion. Targeting these defective trafficking mechanisms offers a novel therapeutic strategy for cancer treatment.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Cell surface proteins are typically degraded via endocytosis.
- Defective endocytic trafficking of receptors and adhesion complexes is a hallmark of cancer.
- Oncogenic alterations impact ubiquitylation, cytoskeletal interactions, and Rab proteins, leading to endocytosis defects.
Purpose of the Study:
- To investigate the role of endocytic pathway defects in cancer.
- To explore the potential of targeting these defects for cancer therapy.
Main Methods:
- Analysis of vesicular trafficking pathways.
- Investigation of growth factor receptor and adhesion complex recycling.
- Examination of ubiquitylation, cytoskeletal interactions, and Rab family members in cancer cells.
Main Results:
- Malignant cells exhibit defective vesicular trafficking and unbalanced recycling of key cell surface proteins.
- Multiple oncogenic alterations contribute to impaired endocytosis, affecting ubiquitylation and Rab proteins.
- Dysfunctional endocytic machinery is implicated in cancer progression.
Conclusions:
- Defective endocytosis is a critical feature of cancer cells.
- Targeting the aberrant endocytic pathways of tumor cells presents a promising new avenue for cancer therapy.
More Related Videos
09:42Assessing Tumor Microenvironment of Metastasis Doorway-Mediated Vascular Permeability Associated with Cancer Cell Dissemination using Intravital Imaging and Fixed Tissue Analysis
Published on: June 26, 2019
08:11Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics
Published on: March 26, 2018
Related Concept Videos
01:35Cancer Cell Migration through Invadopodia
02:30Metastasis
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...
01:20Receptor-mediated Endocytosis
Clathrin-Mediated Endocytosis of LDL
One well-characterized example of receptor-mediated endocytosis is the...
01:39Receptor-mediated Endocytosis
00:58Recycling Endosomes and Transcytosis
The recycling endosome is not a single organelle but an extensively tubulated network of recycling pathways. It functions in storing molecules or transporting them across...
02:40Cancer Stem Cells and Tumor Maintenance
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...