Apoptosis: Its Role in the Development of Malignancies and its Potential as a Novel Therapeutic Target

Abstract

Apoptosis is a highly organized physiologic mechanism of destroying injured and abnormal cells as well as maintaining homeostasis in multicellular organisms. Both the activation and inhibition of apoptosis are tightly controlled. Pharmacologic manipulation of this pathway is a novel therapeutic target in cancer therapy.

Scutellarein ameliorates tongue cancer cells via mitochondria

“…Because many chemotherapeutic drugs could induce apoptosis in malignant cells, apoptosis has currently been a target for developing antitumor drugs [25]. Recently, there is a growing interest in the use of natural materials or naturally occurring substances for the treatment or prevention of cancer because of the few side effects.…”

University of Pittsburgh Graduate Training Program in Breast Cancer Biology and Therapy

“…extra), damaged, and atypical (i.e. neoplastic) cells and can be induced by various physiologic and pathologic stimuli such as UV light, ionizing radiation, dietary carcinogens, and high levels of glucocorticoids [56]. Apoptosis is an active process that is structured and sequential and can be considered an important response to extensive DNA damage [57].…”

Antitumor effect of steroidal tetraoxanes on malignantly transformed human cell lines

“…Međutim, u odsustvu funkcionalnog p53, oštećene ćelije mogu nastaviti ciklus i doći do mitoze, akumulirajući mutacije, koje neće biti kontrolisane na kontrolnim tačkama ćelijskog ciklusa (105,106). Alternativni mehanizam za koji je pokazano da premošćava regulatornu aktivnost p53 jeste preko Mdm2, negativnog regulatora p53.…”

“…Gen Bcl-2 funkcioniše kao glavni inhibitor ćelijske smrti (95,105,110). Ostali članovi ove porodice koji uključuju Bcl-xL, mcl i bag-1, takođe deluju kao inhibitori ćelijske smrti, dok su bad, bax i bik promoteri apoptoze (110).…”

“…Bcl-xL, veliki protein Bcl-2 familije, ponaša se na sličan način kao Bcl-2 (94, 108), a manji proteini, Bcl-XS, i Bak, suprimiraju aktivnost Bcl-2, čineći tako ćelije osetljivim na apotozu (105,115).…”