Apoptosis is an energy-requiring physiological process known as programmed cell death, and apoptosis plays a critical role in embryological development and maintenance of adult tissues. Apoptosis, known as programmed cell death, is a mechanism that controls and destroys cells that the organism does not need, that have completed their biological task or that are damaged at the genetic level. Various diseases occur when the rate of apoptosis is impaired, slowed down or increased. The apoptosis process can be triggered by intracellular signals, such as genotoxic stress, or by extrinsic signals, such as ligands binding to cell surface death receptors. The mechanism of apoptosis involves various proteins and molecules. Deregulation in the mechanism of apoptotic cell death is the hallmark of cancer. Apoptosis alteration is responsible not only for tumor development and progression, but also for tumor resistance to treatments. Most anticancer drugs currently used in clinical oncology exploit intact apoptotic signaling pathways to induce cancer cell death. In this review, the effects of apoptosis on tumor-inducing and tumor suppressor genes and its functional properties in cancer are outlined.
Apoptoz, programlı hücre ölümü olarak bilinen enerji gerektiren fizyolojik bir süreçtir ayrıca apoptoz embriyolojik gelişim ve erişkin dokuların devamlılığında kritik rol oynar. Programlı hücre ölümü olarak bilinen apoptoz, organizmanın ihtiyaç duymadığı, biyolojik görevini tamamlamış ya da hasarlı hücreleri genetik düzeyde de kontrol ederek yok eden bir mekanizmadır. Apoptoz hızının bozulduğu, yavaşladığı veya arttığı durumlarda çeşitli hastalıklar ortaya çıkmaktadır. Apoptosis süreci genotoksik stres gibi hücre içinden gelen sinyaller veya ligandların hücre yüzeyi ölüm reseptörlerine bağlanması gibi dışsal sinyaller tarafından tetiklenebilir. Apoptosis mekanizması, çeşitli proteinleri ve molekülleri içerir. Apoptotik hücre ölümü mekanizmasındaki kuralsızlaştırma, kanserin ayırt edici özelliğidir. Apoptoz değişikliği sadece tümör gelişimi ve ilerlemesinden değil, aynı zamanda tedavilere karşı tümör direncinden de sorumludur. Şu anda klinik onkolojide kullanılan çoğu antikanser ilacı, kanser hücresi ölümünü tetiklemek için bozulmamış apoptotik sinyal yollarından yararlanır. Bu derlemede, apoptosisin tümör indükleyici ve ayrıca tümör baskılayıcı genlerdeki etkileri ve kanserdeki fonksiyonel özellikleri genel hatlarıyla ifade edilmiştir.
Primary Language | Turkish |
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Subjects | Structural Biology |
Journal Section | Review Articles |
Authors | |
Publication Date | April 10, 2023 |
Submission Date | November 27, 2022 |
Published in Issue | Year 2023 Volume: 49 Issue: 1 |
Journal Owner: On behalf of Selçuk University Faculty of Science, Rector Prof. Dr. Hüseyin YILMAZ
Selcuk University Journal of Science Faculty accepts articles in Turkish and English with original results in basic sciences and other applied sciences. The journal may also include compilations containing current innovations.
It was first published in 1981 as "S.Ü. Fen-Edebiyat Fakültesi Dergisi" and was published under this name until 1984 (Number 1-4).
In 1984, its name was changed to "S.Ü. Fen-Edeb. Fak. Fen Dergisi" and it was published under this name as of the 5th issue.
When the Faculty of Letters and Sciences was separated into the Faculty of Science and the Faculty of Letters with the decision of the Council of Ministers numbered 2008/4344 published in the Official Gazette dated 3 December 2008 and numbered 27073, it has been published as "Selcuk University Journal of Science Faculty" since 2009.
It has been scanned in DergiPark since 2016.
Selcuk University Journal of Science Faculty is licensed under a Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) License.