We hypothesise that autophagy may offer an alternative energy source for the enhanced DNA synthesis needed for endoreplication in polyploid cells promoting the survival of these cells. Ergo, it may be inferred that by inhibiting combretastatin induced polyploidy BAF A1 may reduce the long run success of such cells. Beclin 1 was originally cloned in 1998 angiogenesis cancer and plays a key role in recruiting autophagic proteins to the pre autophagosomal structure by reaching the class III form Phosphatidylinositol 3 Kinase /Vps34. Combretastatin induced autophagy was not associated with a change in beclin 1 protein levels in both CT 26 and Caco 2 cells. Similarly, equally arsenic trioxide and resveratrol caused autophagy was not associated with an increase in beclin 1 protein levels. Nevertheless, unlike in HT 1080 cells where continuous combretastatin exposure paid down Bcl 2 protein levels, combretastatin exposure did not reduce Bcl 2 protein levels in Caco 2 cells therefore it is possible that beclin 1 may connect to Bcl 2 to market the autophagic process in these cells. Mitochondrial damage plays a fundamental role in both apoptosis and autophagy for example depolarisation of the mitochondria can cause apoptotic cell death. But rapid engulfment by the autophagosome may prolong cell survival and prevent apoptotic signals. A recent report Organism highlighted the value of mitochondrial morphology as a determinant of cellular reaction to autophagy. In greater detail, during hunger caused autophagy the mitochondria elongate and possess increased cristae occurrence which favours oligomerisation of ATPase and maintenance of ATP generation allowing the survival of the starving cell. Aberrant mitochondrial morphology including mitochondrial elongation was also observed in our study in CT 26 cells considering combretastatin caused autophagy. This finding would suggest that mitochondria also combine under stress caused autophagy. A moderate but signifi GS-1101 distributor cant decrease was induced by the combretastatins in mitochondrial membrane potential relative to control cells. It’s been postulated that moderate mitochondrial damage might stimulate autophagic destruction of such organelles and prevent apoptotic signals. We hypothe sise that the rapid elimination of small damaged mitochondria by the autophagosome may delay the onset of apoptotic signals which together with an upsurge in pointed more energy efficient mitochondria may increase the success of CT 26 cells carrying out a prolonged experience of combretastatins. To date, the membrane source of the autophagosomes is just a long standing issue. A few independent studies propose the membrane and supporting structures may possibly result from pre current organelles.