» Articles » PMID: 20182539

Evasion of Apoptosis As a Cellular Stress Response in Cancer

Overview
Journal Int J Cell Biol
Publisher Wiley
Specialty Cell Biology
Date 2010 Feb 26
PMID 20182539
Citations 68
Authors
Affiliations
Soon will be listed here.
Abstract

One of the hallmarks of human cancers is the intrinsic or acquired resistance to apoptosis. Evasion of apoptosis can be part of a cellular stress response to ensure the cell's survival upon exposure to stressful stimuli. Apoptosis resistance may contribute to carcinogenesis, tumor progression, and also treatment resistance, since most current anticancer therapies including chemotherapy as well as radio- and immunotherapies primarily act by activating cell death pathways including apoptosis in cancer cells. Hence, a better understanding of the molecular mechanisms regarding how cellular stress stimuli trigger antiapoptotic mechanisms and how this contributes to tumor resistance to apoptotic cell death is expected to provide the basis for a rational approach to overcome apoptosis resistance mechanisms in cancers.

Citing Articles

Exploring natural products as apoptosis modulators in cancers: insights into natural product-based therapeutic strategies.

Utpal B, Bouenni H, Zehravi M, Sweilam S, Mortuza M, Arjun U Naunyn Schmiedebergs Arch Pharmacol. 2025; .

PMID: 40014131 DOI: 10.1007/s00210-025-03876-8.


Enhancement of the Sensitivity of the Acute Lymphoblastic Leukemia Cells to ABT-737 by Formononetin.

Abbasi Y, Pooladi M, Nazmabadi R, Amri J, Abbasi H, Aghabeygi R Int J Mol Cell Med. 2024; 13(3):259-271.

PMID: 39493513 PMC: 11530950. DOI: 10.22088/IJMCM.BUMS.13.3.259.


Novel Thienopyrimidine-Hydrazinyl Compounds Induce DRP1-Mediated Non-Apoptotic Cell Death in Triple-Negative Breast Cancer Cells.

Malla S, Nyinawabera A, Neupane R, Pathak R, Lee D, Abou-Dahech M Cancers (Basel). 2024; 16(15).

PMID: 39123351 PMC: 11311031. DOI: 10.3390/cancers16152621.


Harnessing the potential of hydrogels for advanced therapeutic applications: current achievements and future directions.

Lu P, Ruan D, Huang M, Tian M, Zhu K, Gan Z Signal Transduct Target Ther. 2024; 9(1):166.

PMID: 38945949 PMC: 11214942. DOI: 10.1038/s41392-024-01852-x.


Necroptosis induced by ruthenium (II) complexes as mitochondrial disruptors.

Goncalves J, Amaral J, Capela R, Perry M, Braga C, Gaspar M Cell Death Discov. 2024; 10(1):261.

PMID: 38806468 PMC: 11133381. DOI: 10.1038/s41420-024-02033-z.


References
1.
Weston C, Davis R . The JNK signal transduction pathway. Curr Opin Cell Biol. 2007; 19(2):142-9. DOI: 10.1016/j.ceb.2007.02.001. View

2.
Schafer Z, Kornbluth S . The apoptosome: physiological, developmental, and pathological modes of regulation. Dev Cell. 2006; 10(5):549-61. DOI: 10.1016/j.devcel.2006.04.008. View

3.
Willis S, Fletcher J, Kaufmann T, van Delft M, Chen L, Czabotar P . Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak. Science. 2007; 315(5813):856-9. DOI: 10.1126/science.1133289. View

4.
Sturm I, Bosanquet A, Radetzki S, Hummel M, Dorken B, Daniel P . Silencing of APAF-1 in B-CLL results in poor prognosis in the case of concomitant p53 mutation. Int J Cancer. 2005; 118(9):2329-36. DOI: 10.1002/ijc.21535. View

5.
Clement M, Hirpara J, Pervaiz S . Decrease in intracellular superoxide sensitizes Bcl-2-overexpressing tumor cells to receptor and drug-induced apoptosis independent of the mitochondria. Cell Death Differ. 2003; 10(11):1273-85. DOI: 10.1038/sj.cdd.4401302. View