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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...

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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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Related Experiment Video

Updated: Jun 5, 2026

Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment

Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment

Published on: November 23, 2017

Secreting tumor suppression.

Yuchen Chien¹, Scott W Lowe

¹Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.

|February 13, 2008

Summary

This summary is machine-generated.

Cellular senescence, a tumor suppressor mechanism, involves insulin-like growth factor binding protein 7 (IGFBP7). This protein mediates oncogene-induced senescence in melanocytes and triggers apoptosis in melanoma cells, offering a novel therapeutic strategy.

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Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment

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Published on: November 28, 2019

Area of Science:

Oncology
Cell Biology
Molecular Medicine

Background:

Cellular senescence is a key tumor suppressor mechanism that limits the proliferation of damaged cells.
Oncogenic mutations, such as BRAF, can disrupt normal cellular processes and lead to cancer development.

Purpose of the Study:

To identify secreted factors involved in oncogene-induced senescence in normal melanocytes.
To investigate the role of these factors in melanoma progression and explore potential therapeutic applications.

Main Methods:

Utilized gene expression analysis and proteomic techniques to identify secreted proteins.
Employed cell culture models of normal melanocytes and melanoma.
Investigated the effects of the identified factor on senescence induction and apoptosis.

Main Results:

Identified insulin-like growth factor binding protein 7 (IGFBP7) as a secreted factor mediating senescence induced by oncogenic BRAF in normal melanocytes.
Demonstrated that IGFBP7 triggers apoptosis in melanoma cells that have progressed beyond senescence.

Conclusions:

IGFBP7 is a novel mediator of oncogene-induced senescence in melanocytes.
IGFBP7 represents a potential therapeutic target for melanoma treatment by inducing apoptosis in cancer cells.