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Updated: Jul 10, 2026

Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics
Published on: March 26, 2018
Aberrant receptor signaling and trafficking as mechanisms in oncogenesis
Kaisa Haglund1, Tor Erik Rusten, Harald Stenmark
1Centre for Cancer Biomedicine, University of Oslo, and Department of Biochemistry, Institute for Cancer Research, the Norwegian Radium Hospital, Montebello, 0310 Oslo, Norway.
Abstract:
Intracellular signaling pathways activated through cell surface receptors are essential for cell proliferation, differentiation, survival, and migration. Dysregulation of such signaling through mutations, chromosome rearrangements, aberrant gene expression, or epigenetic changes is a key factor in oncogenesis. Prominent examples of receptor signaling pathways that are dysregulated in cancers include those initiated by receptor tyrosine kinases, WNT, TGFbeta, and Notch receptors. In this review we will discuss these signaling pathways and how their dysfunction may contribute to oncogenesis. We will also highlight the important role of endocytic membrane trafficking in receptor signaling and tumor suppression.
Insights
Cell surface receptor signaling pathways are crucial for normal cell functions. Their dysregulation in cancer, involving pathways like WNT and Notch, drives oncogenesis, with endocytic trafficking playing a key role.
Area of Science:
- Cell Biology
- Molecular Oncology
- Cancer Research
Background:
- Cell surface receptor signaling pathways regulate fundamental cellular processes like proliferation, differentiation, survival, and migration.
- Aberrant signaling, driven by genetic or epigenetic alterations, is a critical mechanism in cancer development (oncogenesis).
Purpose of the Study:
- To review key cell surface receptor signaling pathways dysregulated in cancer, including receptor tyrosine kinases, WNT, TGF-beta, and Notch.
- To elucidate the contribution of these pathway dysfunctions to oncogenesis.
- To highlight the role of endocytic membrane trafficking in both receptor signaling and tumor suppression.
Main Methods:
- Literature review of prominent receptor signaling pathways in cancer.
- Analysis of mechanisms linking pathway dysfunction to oncogenesis.
- Examination of the role of endocytic trafficking in receptor signaling and tumor suppression.
Main Results:
- Dysregulation of receptor tyrosine kinases, WNT, TGF-beta, and Notch signaling pathways is frequently observed in various cancers.
- These dysregulated pathways promote uncontrolled cell growth, survival, and metastasis, key hallmarks of cancer.
- Endocytic membrane trafficking is integral to the regulation of receptor signaling and functions as a tumor suppressor mechanism.
Conclusions:
- Understanding the specific roles of dysregulated signaling pathways and endocytic trafficking is crucial for developing targeted cancer therapies.
- Targeting these pathways offers potential therapeutic strategies for oncogenesis.
- Further research into the interplay between receptor signaling and endocytic trafficking may reveal novel avenues for cancer treatment.
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