Dying cells encourage neighbors to grow

October 05, 2004

Researchers from The Rockefeller University have uncovered specific mechanisms by which cells that are genetically programmed to commit suicide stimulate growth in surrounding cells. The research, published online in Developmental Cell, provides new information about how normal, healthy tissues are maintained and may shed some light on a pathway that may contribute to tumor growth.

It has been known for some time that cells that die as a result of injury-provoked programmed cell death, also known as apoptosis, may stimulate the growth of surrounding cells. "Such compensatory mechanisms may be essential to allow for the elimination of as many damaged or dangerous cells as needed without compromising organismal fitness. In spite of its importance, the underlying mechanisms are poorly understood," explains study leader Dr. Hermann Steller.

Dr. Steller and colleagues demonstrate that when cells from the imaginal disc in the fruit fly Drosophila are stimulated to undergo apoptosis but experimentally manipulated so that they do not actually die ("undead cells"), they stimulate the growth of neighboring tissue. The researchers demonstrate that the undead cells promote cell growth in the surrounding imaginal disc by activating specific signaling cascades that are known to be required for cell proliferation. Although artificial, the experimental creation of undead cells allows this phenomenon to be expanded and studied. The authors provide evidence that apoptotic cells that are allowed to complete the process of dying also secrete the growth-stimulating signals.

The researchers conclude that apoptotic cells actively induce compensatory proliferation by activating growth-associated signaling pathways and secreting molecules that promote growth in surrounding tissues. They also suggest that abnormal regulation of apoptosis, as has been shown to be the case in some cancers, may result in pathological activation of these pathways. "Based on the behavior of undead cells in Drosophila imaginal discs, one might expect mutations that block or delay apoptosis to cause secondary proliferation and hyperplasia. It remains to be tested if such a mechanism contributes to hyperplasia in mouse models and human malignancies," offers Dr. Steller.
-end-
Hyung Don Ryoo, Travis Gorenc, and Hermann Steller: "Apoptotic Cells Can Induce Compensatory Cell Proliferation through the JNK and the Wingless Signaling Pathways"

Publishing in Developmental Cell, Volume 7, Number 4, October 2004, pages 491-501.

Cell Press

Related Apoptosis Articles from Brightsurf:

Thymoquinone induces apoptosis & DNA damage in 5-Fluorouracil-resistant colorectal cancer
Volume 11, Issue 31 from @Oncotarget reported that TQ decreased the expression levels of colorectal stem cell markers CD44 and Epithelial Cell Adhesion Molecule Ep CAM and proliferation marker Ki67 in colonospheres derived from both cell lines and reduced cellular migration and invasion.

Oncotarget: Th1 cytokines potentiate apoptosis of breast cancer cells and suppress tumor growth
Volume 11, Issue 30 of Oncotarget reported that previously, the authors showed that anti-estrogen drugs combined with a dendritic cell-based anti-HER-2 vaccine known to induce strong Th1-polarized immunity dramatically improved clinical response rates in patients with HER-2pos/ERpos early breast cancer.

Opening an autophagy window as the apoptosis door starts to close
Tokyo Medical and Dental University (TMDU) researchers have successfully attached the cancer cell-targeting antibody Trastuzumab to a previously reported supermolecule that induces autophagic cell death.

Stop Livin to make lymphoma cells stop living
Researchers at the University of Tsukuba have shown that the protein Livin, an inhibitor of apoptosis or programmed cell death, mediates resistance to immunotherapy in some lymphoma variants.

Protein causes mutations that lead to breast cancer cell aggression
In her previous research, University of Alberta biochemist Ing Swie Goping identified that the protein, BCL-2 interacting killer (BIK), was associated with relapses in breast cancer patients.

Shigella prevents infected cells from sacrificing themselves for the greater good
Researchers from Tokyo Medical and Dental University (TMDU) investigated how Shigella survive and multiply to cause severe inflammatory colitis.

Bacteria can 'outsmart' programmed cell death
To be able to multiply, bacteria that cause diarrhoea block mediators of programmed cell death, a new study in 'Nature Microbiology' shows.

High expression of apoptosis protein (Api-5) in chemoresistant triple-negative breast cancers: an innovative target
78 TNBC biopsies from patients with different responses to chemotherapy were analysed for API-5 expression before any treatment.

High expression of apoptosis protein (Api-5) in chemoresistant triple-negative breast cancers
78 TNBC biopsies from patients with different responses to chemotherapy were analysed for API-5 expression before any treatment.

Researchers describe a mechanism inducing self-killing of cancer cells
A KAIST research team has developed helical polypeptide potassium ionophores that lead to the onset of programmed cell death.

Read More: Apoptosis News and Apoptosis Current Events
Brightsurf.com is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to Amazon.com.