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Apoptosis is a multi-step, multi-pathway cell-death programme that is inherent in every cell of the body. In cancer, the apoptosis cell-division ratio is altered. Cancer treatment by chemotherapy and irradiation kills target cells primarily by inducing apoptosis. [97]
Not only does the peptide have a reduced hemolytic action, it also is semi-selective towards cancer cells and leaves non-cancerous cells largely unharmed. This peptide works to prevent the progression of cancer by arresting the cell cycle at the G2/M phase, resulting in an induction of apoptosis.
The combinations of the domains in the proteins determine its role in the apoptosis process. Members of the family that inhibit apoptosis include Bcl-2 itself, Bcl-XL, and Bcl-w, which possess all four of the domains. [3] Bcl-2 is the most well known of the anti-apoptotic members, and is classified as an oncogene. Studies have shown that the ...
Cancer can be seen as a disturbance in the homeostatic balance between cell growth and cell death. Over-expression of anti-apoptotic genes, and under-expression of pro-apoptotic genes, can result in the lack of cell death that is characteristic of cancer. An example can be seen in lymphomas. The over-expression of the anti-apoptotic Bcl-2 ...
Many tumor suppressors work to regulate the cycle at specific checkpoints in order to prevent damaged cells from replicating. A tumor suppressor gene (TSG), or anti-oncogene, is a gene that regulates a cell during cell division and replication. [1] If the cell grows uncontrollably, it will result in cancer. When a tumor suppressor gene is ...
APO-1-mediated apoptosis can be inhibited by a variety of factors, including the viral caspase inhibitors CrmA and p35, as well as viral FLICE-inhibitory proteins known as v-FLIPs. When in the presence of APO-1, v-FLIPs preferentially bind and prevent procaspase-8 from being recruited; as such, apoptosis is stalled.
The cancer cells may do this by altering the mechanisms that detect the damage or abnormalities. This means that proper signaling cannot occur, thus apoptosis cannot activate. They may also have defects in the downstream signaling itself, or the proteins involved in apoptosis, each of which will also prevent proper apoptosis. [4] [8]
PUMA has been shown to be active in inducing apoptosis in hematopoietic and intestinal tissue following γ-irradiation. [12] [55] Since inhibition of PUMA does not directly cause spontaneous malignancies, therapeutics to inhibit PUMA function in healthy tissue could lessen or eliminate the side effects of traditional cancer therapies. [7]