Programmed Cell Death in Cancer Cells

Česká verzia

Authors: E. Ondroušková; B. Vojtěšek
Authors place of work: Regionální centrum aplikované molekulární onkologie, Masarykův onkologický ústav, Brno
Published in the journal: Klin Onkol 2014; 27(Supplementum): 7-14

Summary

Resistance to programmed cell death is one of the hallmarks of cancer cells that affects the process of malignant transformation as well as response to cancer therapy. The goal of this review is to summarize recent information about programmed cell death (PCD) in healthy and cancer cells, as well as new perspectives for anticancer treatments targeting these signaling pathways. Three main types of PCD are described in detail: apoptosis, necrosis/ necroptosis and cell death associated with autophagy. Among them, apoptosis plays the key role in both malignant transformation and response to therapy. In this review, we describe main signaling pathways and molecules participating in apoptosis regulation in healthy cells. In most cancer cells, mutations or aberrant expression of proteins directly or indirectly involved in induction and execution of cell death can be detected – p53, Bcl‑ 2 family proteins, inhibitors of apoptosis, death receptors/ ligands and other proteins. Mutations or changes in expression of these proteins and their relation to certain types of tumors are described. Finally, we provide a review of recently developed treatments that target and reactivate the machinery of programmed cell death and are currently tested in clinical trials.

Key words:
programmed cell death – apoptosis – necroptosis – autophagy – caspases – Bcl‑ 2

This work was supported by the European Regional Development Fund and the State Budget of the Czech Republic (RECAMO, CZ.1.05/2.1.00/03.0101) and by MH CZ – DRO (MMCI, 00209805).

The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.

The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers.

Submitted:
14. 1. 2014

Accepted:
6. 3. 2014

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