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Articles de revues sur le sujet « Cell death »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 9 juin 2025

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1

Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

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Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.

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2

Lockshin, Richard A., and Zahra Zakeri. "Cell Death (Apoptosis, Programmed Cell Death)." Directions in Science 1 (February 27, 2002): 41–44. http://dx.doi.org/10.1100/tsw.2002.161.

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3

Yao, Nan, and Jean T. Greenberg. "Arabidopsis ACCELERATED CELL DEATH2 Modulates Programmed Cell Death." Plant Cell 18, no. 2 (December 30, 2005): 397–411. http://dx.doi.org/10.1105/tpc.105.036251.

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4

Deniz, Özdemir. "KAN0438757: A NOVEL PFKFB3 INHIBITOR THAT INDUCES PROGRAMMED CELL DEATH AND SUPPRESSES CELL MIGRATION IN NON-SMALL CELL LUNG CARCINOMA CELLS." Biotechnologia Acta 16, no. 5 (October 31, 2023): 34–44. http://dx.doi.org/10.15407/biotech16.05.034.

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Aim. PFKFB3 is glycolytic activators that is overexpressed in human lung cancer and plays a crucial role in multiple cellular functions including programmed cell death. Despite the many small molecules described as PFKFB3 inhibitors, some of them have shown disappointing results in vitro and in vivo. On the other hand KAN0438757, selective and potent, small molecule inhibitor has been developed. However, the effects of KAN0438757, in non-small cell lung carcinoma cells remain unknown. Herein, we sought to decipher the effect of KAN0438757 on proliferation, migration, DNA damage, and programmed cell death in non-small cell lung carcinoma cells. Methods. The effects of KAN0438757 on cell viability, proliferation, DNA damage, migration, apoptosis, and autophagy in in non-small cell lung carcinoma cells was tested by WST-1, real-time cell analysis, comet assay, wound-healing migration test, and MMP/JC-1 and AO/ER dual staining assays as well as western blot analysis. Results. Our results revealed that KAN0438757 significantly suppressed the viability and proliferation of A549 and H1299 cells and inhibited migration of A549 cells. More importantly, KAN0438757 caused DNA damage and triggered apoptosis and this was accompanied by the up-regulation of cleaved PARP in A549 cells. Furthermore, treatment with KAN0438757 resulted in increased LC3 II and Beclin1, which indicated that KAN0438757 stimulated autophagy. Conclusions. Overall, targeting PFKFB3 with KAN0438757 may be a promising effective treatment approach, requiring further in vitro and in vivo evaluation of KAN0438757 as a therapy in non-small cell lung carcinoma cells.

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5

Sarosiek, Kristopher. "Blocking cell death to enhance cell death." Science Translational Medicine 9, no. 408 (September 20, 2017): eaao6129. http://dx.doi.org/10.1126/scitranslmed.aao6129.

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6

M, Aloysius Dhivya, Kishore A, and Bharathidevi SR. "Down-Regulation of NRF2 Signaling Triggers Cell Death in Y79 Cells upon Copper Chelation." Open Access Journal of Ophthalmology 10, no. 1 (2025): 1–10. https://doi.org/10.23880/oajo-16000329.

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Background: Retinoblastoma is a rare intraocular malignancy that leads to vision loss in children. While copper (Cu) chelation has been reported as a therapy in many cancers, its relevance to retinoblastoma has not yet been explored. Objectives: In this study, we have explored the role of penicillamine (a Cu chelator) as a therapeutic target for retinoblastoma using Y79 cells as a model. Methods: The effect of the Cu chelator on the viability of Y79 was assessed using the MTT assay. Additionally, we performed nuclear fractionation to assess Nuclear factor erythroid 2–related factor 2 (NRF2) activation, evaluated the downstream targets of NRF2 at transcript and protein levels, and measured SOD (superoxide dismutase) activity. Results: Penicillamine (2 mM) induced cell death in Y79 cells, inhibited NRF2 signaling, and reduced SOD activity. Furthermore, the downstream targets of NRF2 namely VEGF as well as PCNA (proliferating cell nuclear antigen) were decreased with penicillamine, which induced cell death in Y79 cells. We observed similar results in HeLa cells (positive control) comparable to Y79 cells. Conclusion: Therefore, we speculate that penicillamine could be a target for retinoblastoma as it induces cell death in Y79 cells by regulating NRF2 nuclear translocation and decreasing its downstream targets.

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7

Medema, J. P., H. Walczak, M. Hahne, and V. de Laurenzi. "Cell Death." Cell Death & Differentiation 17, no. 4 (March 15, 2010): 730–32. http://dx.doi.org/10.1038/cdd.2010.11.

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8

Hotchkiss, Richard S., Andreas Strasser, Jonathan E. McDunn, and Paul E. Swanson. "Cell Death." New England Journal of Medicine 361, no. 16 (October 15, 2009): 1570–83. http://dx.doi.org/10.1056/nejmra0901217.

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9

Vogel, Michael W. "Cell Death." American Journal of Psychiatry 162, no. 8 (August 2005): 1503. http://dx.doi.org/10.1176/appi.ajp.162.8.1503.

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10

MALORNI, WALTER, and GIANFRANCO DONELLI. "Cell Death." Annals of the New York Academy of Sciences 663, no. 1 Aging and Cel (November 1992): 218–33. http://dx.doi.org/10.1111/j.1749-6632.1992.tb38666.x.

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11

Giampietri, Claudia, Alessio Paone, and Alessio D’Alessio. "Cell Death." International Journal of Cell Biology 2014 (2014): 1–2. http://dx.doi.org/10.1155/2014/864062.

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12

Danial, Nika N., and Stanley J. Korsmeyer. "Cell Death." Cell 116, no. 2 (January 2004): 205–19. http://dx.doi.org/10.1016/s0092-8674(04)00046-7.

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13

Newton, Kim, Andreas Strasser, Nobuhiko Kayagaki, and Vishva M. Dixit. "Cell death." Cell 187, no. 2 (January 2024): 235–56. http://dx.doi.org/10.1016/j.cell.2023.11.044.

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14

Klishch, M., N. Skorokhyd, R. Panchuk, and R. Stoika. "Biochemical and cellular mechanisms of immunogenic cell death." Ukrainian Biochemical Journal 96, no. 6 (December 12, 2024): 5–16. https://doi.org/10.15407/ubj96.06.005.

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Immunogenic cell death (ICD) is a mode of programmed cell death that leads to the activation of anticancer immune response and determines the long-term success of anticancer therapies. Here, we provide a review of the known molecular and cellular mechanisms of ICD. Usually, solid tumor experimental models have been used in ICD studies. However, ascites tumor models may possess some advantages over them. The results of our investigation on the approbation of murine Nemeth-Kellner lymphoma as an experimental ascites tumor model for ICD studies are presented. Keywords: ascites tumor model, biochemical mechanisms, doxorubicin, immunogenic cell death, murine Nemeth-Kellner lymphoma, oxaliplatin

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15

Momoi, Takashi. "Conformational Diseases and ER Stress-Mediated Cell Death: Apoptotic Cell Death and Autophagic Cell Death." Current Molecular Medicine 6, no. 1 (February 1, 2006): 111–18. http://dx.doi.org/10.2174/156652406775574596.

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16

Panaretakis, T., L. Hjortsberg, J. M. R. Lambert, and B. Joseph. "Second Cell Death Network symposium: the vital cell death." Cell Death & Differentiation 16, no. 9 (August 17, 2009): 1300–1302. http://dx.doi.org/10.1038/cdd.2009.93.

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17

Imig, Dirke, Karsten Kuritz, Nadine Pollak, Markus Rehm, and Frank Allgöwer. "Death patterns resulting from cell cycle-independent cell death." IFAC-PapersOnLine 51, no. 19 (2018): 90–93. http://dx.doi.org/10.1016/j.ifacol.2018.09.028.

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18

Maddox, Amy Shaub, and Jan M. Skotheim. "Cell cycle, cell division, cell death." Molecular Biology of the Cell 30, no. 6 (March 15, 2019): 732. http://dx.doi.org/10.1091/mbc.e18-12-0819.

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19

Miura, Masayuki, Shin Hisahara, Riya Takano, Shin'ichi Shoji, and Hideyuki Okano. "Oligodendrocyte cell death by death factors." Neuroscience Research 31 (January 1998): S53. http://dx.doi.org/10.1016/s0168-0102(98)81804-x.

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20

Samali, Afshin, Simone Fulda, Adrienne M. Gorman, Osamu Hori, and Srinivasa M. Srinivasula. "Cell Stress and Cell Death." International Journal of Cell Biology 2010 (2010): 1–2. http://dx.doi.org/10.1155/2010/245803.

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21

Roy, Arun K. "Cell ageing and cell death." Trends in Biochemical Sciences 10, no. 9 (September 1985): 371–72. http://dx.doi.org/10.1016/0968-0004(85)90124-0.

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22

Pillai, Harikrishna, Anuraj K. S. Anuraj K.S, and Harikumar S. Kartha. "Guanine Nucleotide Oxidation and Cell Death by Bactericidal Antibiotics." Global Journal For Research Analysis 3, no. 7 (June 15, 2012): 273–74. http://dx.doi.org/10.15373/22778160/july2014/98.

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23

Neves, A. A., and K. M. Brindle. "Imaging Cell Death." Journal of Nuclear Medicine 55, no. 1 (January 1, 2014): 1–4. http://dx.doi.org/10.2967/jnumed.112.114264.

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24

Fulton, Alice B. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20. http://dx.doi.org/10.1126/science.274.5284.20.b.

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25

Novak, Jan. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20. http://dx.doi.org/10.1126/science.274.5284.20.a.

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26

Cahill, Larry, and Henry J. Haigler. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1251. http://dx.doi.org/10.1126/science.272.5266.1251.a.

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27

Zaidel, Dahlia W., and Margaret M. Esiri. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1249. http://dx.doi.org/10.1126/science.272.5266.1249.a.

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28

Landfield, Philip W., Bruce S. McEwen, Robert M. Sapolsky, and Michael J. Meaney. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1249–51. http://dx.doi.org/10.1126/science.272.5266.1249.b.

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29

Cahill, Larry, and Henry J. Haigler. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1251. http://dx.doi.org/10.1126/science.272.5266.1251-a.

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30

Landfield, Philip W., Bruce S. McEwen, Robert M. Sapolsky, and Michael J. Meaney. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1249–51. http://dx.doi.org/10.1126/science.272.5266.1249-b.

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31

Zaidel, Dahlia W., and Margaret M. Esiri. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1249. http://dx.doi.org/10.1126/science.272.5266.1249-a.

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32

Green, Douglas R., and Fabien Llambi. "Cell Death Signaling." Cold Spring Harbor Perspectives in Biology 7, no. 12 (December 2015): a006080. http://dx.doi.org/10.1101/cshperspect.a006080.

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33

David, Rachel. "'Cheating' cell death." Nature Reviews Molecular Cell Biology 11, no. 7 (June 9, 2010): 462–63. http://dx.doi.org/10.1038/nrm2922.

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34

Garg, Abhishek D., Aleksandra M. Dudek-Peric, Erminia Romano, and Patrizia Agostinis. "Immunogenic cell death." International Journal of Developmental Biology 59, no. 1-2-3 (2015): 131–40. http://dx.doi.org/10.1387/ijdb.150061pa.

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35

Greenwood, Emma. "Survivin' cell death." Nature Reviews Cancer 1, no. 2 (November 2001): 97. http://dx.doi.org/10.1038/35101029.

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36

Sinclair, Meeghan. "Modeling cell death." Nature Biotechnology 18, no. 7 (July 2000): 703. http://dx.doi.org/10.1038/77234.

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37

Zaidel, D. W., M. M. Esiri;, P. W. Landfield, B. S. McEwen, R. M. Sapolsky, M. J. Meaney;, L. Cahill, and H. J. Haigler. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1247d—1251. http://dx.doi.org/10.1126/science.272.5266.1247d.

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38

Zaidel, D. W., and M. M. Esiri. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1249a. http://dx.doi.org/10.1126/science.272.5266.1249a.

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39

Landfield, P. W., B. S. McEwen, R. M. Sapolsky, and M. J. Meaney. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1249b—1251b. http://dx.doi.org/10.1126/science.272.5266.1249b.

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40

Cahill, L., and H. J. Haigler. "Hippocampal Cell Death." Science 272, no. 5266 (May 31, 1996): 1251a. http://dx.doi.org/10.1126/science.272.5266.1251a.

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41

Medema, Jan Paul, Michael Hahne, Henning Walczak, and Vincenzo De Laurenzi. "Rocking cell death." Cell Death & Differentiation 6, no. 3 (March 1999): 297–300. http://dx.doi.org/10.1038/sj.cdd.4400480.

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42

Seçer, Merve Nur Şahan, and Mine Dosay-Akbulut. "Cell Death Mechanisms." Journal of Advances in Biology & Biotechnology 27, no. 11 (November 4, 2024): 241–70. http://dx.doi.org/10.9734/jabb/2024/v27i111609.

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Cells and their building blocks ensure the maintenance of life by performing complex tasks such as taking in nutrients, excreting waste materials, producing energy, growth, division and reproduction. The form of intercellular communication and coordination is critical for the organism to grow, develop, and adapt to its environment optimally. The numerical balance of the cells that make up the organism is very important for it to survive in a healthy way. While new cells are being created in the living being, some of the existing cells are also eliminated through cell death, thus ensuring a stable balance. As new cells are generated within the organism, a portion of the existing cells undergoes elimination through the process of cell death, thereby maintaining a stable balance. To uphold this mechanism, various forms of cell death mechanisms are activated. Cell death occurs spontaneously, genetically or by other factors that are a part of the life of living things. It basically exists in two main forms. These are programmed and unprogrammed cell death. Cell death mechanisms are critical for the development, survival and health of living organisms. This process, which is basically divided into two main categories, is called programmed cell death (apoptosis) and unprogrammed cell death (necrosis). Programmed and unprogrammed cell death mechanisms are very important for the proper functioning of biological systems and the continuation of life. While programmed cell death (apoptosis) plays very important roles in the regulation and development of tissues, homeostasis, immune response and prevention of diseases, unprogrammed cell death (necrosis) is important in the rapid repair of tissue by clearing damaged cells and the clearance of pathogens. Understanding the way death mechanisms work is very important in terms of understanding the effects that may occur on a healthy continuation of life and in developing more effective methods in the treatment of diseases that may arise as a result. For these reasons, what death mechanisms are, their types, differences and working principles have been tried to be summarized in this study.

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43

Adler, E. M. "Silencing Cell Death?" Science Signaling 2007, no. 389 (June 5, 2007): tw192. http://dx.doi.org/10.1126/stke.3892007tw192.

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44

Cory, S. "Cell death throes." Proceedings of the National Academy of Sciences 95, no. 21 (October 13, 1998): 12077–79. http://dx.doi.org/10.1073/pnas.95.21.12077.

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45

Novak, J., A. B. Fulton, and J. C. Ameisen. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 17–21. http://dx.doi.org/10.1126/science.274.5284.17c.

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46

Novak, J. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20. http://dx.doi.org/10.1126/science.274.5284.20.

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47

Fulton, A. B. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20. http://dx.doi.org/10.1126/science.274.5284.20-a.

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48

Novak, J. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20a. http://dx.doi.org/10.1126/science.274.5284.20a.

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49

Fulton, A. B. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20b. http://dx.doi.org/10.1126/science.274.5284.20b.

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50

Golstein, P. "Controlling Cell Death." Science 275, no. 5303 (February 21, 1997): 1081–82. http://dx.doi.org/10.1126/science.275.5303.1081.

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