engleski

Interaction between cell death and cell proliferation in cancer

Apotosis is molecularly regulated and genetically programmed cell death. It can be induced by a range of environmental, physical or chemical stresses. It is characterised by sequence of precisely regulated events that culminate in self-destruction of a cell. Apotosis is a common phenomenon in developmental processes and in normal physiological conditions when unnecessary cells have to be eliminated. There are many biochemical and genetic parallels between cell death pathways in different animal species. Apotosis is also the predominant form of cell death triggered by cytotoxic drugs in tumour cells. Cellular survival under the stressful environmental conditions is also genetically programmed and mediated by the activity of physiological defence mechanisms. That is another, even more conserved and evolutionarily ancient cellular response. This response is mediated by the heat shock proteins (Hsp). Hsp is highly conserved family of proteins that play a major role in cytoprotection. However, apoptosis that is induced to eliminate unwanted, damaged or old cells may be understood as another way of protecting tissues, from the great changes in the environment. Consequently, there are many functional interactions between these two mechanistically opposing, mechanisms that regulate the cellular decision to live or to die. Recent studies have established that the survival-promoting effects of Hsp can be partially attributed to the suppression of apoptosis. Therefore there is a great potential in pharmacological applications of Hsp inhibitors that may help inducing apoptosis when that may be beneficial, as in various tumours.

apoptosis; heat shock proteins

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