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Journal articles on the topic 'Cancer research; Cell death'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Catalano, Veronica, Miriam Gaggianesi, Valentina Spina, Flora Iovino, Francesco Dieli, Giorgio Stassi, and Matilde Todaro. "Colorectal Cancer Stem Cells and Cell Death." Cancers 3, no. 2 (April 11, 2011): 1929–46. http://dx.doi.org/10.3390/cancers3021929.

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2

Brancolini, Claudio, and Luca Iuliano. "Proteotoxic Stress and Cell Death in Cancer Cells." Cancers 12, no. 9 (August 23, 2020): 2385. http://dx.doi.org/10.3390/cancers12092385.

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To maintain proteostasis, cells must integrate information and activities that supervise protein synthesis, protein folding, conformational stability, and also protein degradation. Extrinsic and intrinsic conditions can both impact normal proteostasis, causing the appearance of proteotoxic stress. Initially, proteotoxic stress elicits adaptive responses aimed at restoring proteostasis, allowing cells to survive the stress condition. However, if the proteostasis restoration fails, a permanent and sustained proteotoxic stress can be deleterious, and cell death ensues. Many cancer cells convive with high levels of proteotoxic stress, and this condition could be exploited from a therapeutic perspective. Understanding the cell death pathways engaged by proteotoxic stress is instrumental to better hijack the proliferative fate of cancer cells.

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3

Zhu, Shan, Qiuhong Zhang, Xiaofan Sun, Herbert J. Zeh, Michael T. Lotze, Rui Kang, and Daolin Tang. "HSPA5 Regulates Ferroptotic Cell Death in Cancer Cells." Cancer Research 77, no. 8 (January 27, 2017): 2064–77. http://dx.doi.org/10.1158/0008-5472.can-16-1979.

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4

Philchenkov, Alex. "Preface: Focus on Cell Death." Critical Reviews™ in Oncogenesis 21, no. 3-4 (2016): v—vii. http://dx.doi.org/10.1615/critrevoncog.2016017027.

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5

Macintosh, Robin L., and Kevin M. Ryan. "Autophagy in tumour cell death." Seminars in Cancer Biology 23, no. 5 (October 2013): 344–51. http://dx.doi.org/10.1016/j.semcancer.2013.05.006.

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6

Sonnenschein, Carlos, and Ana M. Soto. "The Death of the Cancer Cell." Cancer Research 71, no. 13 (April 20, 2011): 4334–37. http://dx.doi.org/10.1158/0008-5472.can-11-0639.

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7

Carpinteiro, Alexander, Claudia Dumitru, Marcus Schenck, and Erich Gulbins. "Ceramide-induced cell death in malignant cells." Cancer Letters 264, no. 1 (June 2008): 1–10. http://dx.doi.org/10.1016/j.canlet.2008.02.020.

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8

Wang, Tzu-Hao, Hsin-Shih Wang, and Yung-Kwei Soong. "Paclitaxel-induced cell death." Cancer 88, no. 11 (June 1, 2000): 2619–28. http://dx.doi.org/10.1002/1097-0142(20000601)88:11<2619::aid-cncr26>3.0.co;2-j.

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9

Greenwood, Emma. "MUCking up cell death." Nature Reviews Cancer 4, no. 4 (April 2004): 249. http://dx.doi.org/10.1038/nrc1325.

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10

Bangham, Jenny. "Checking in cell death." Nature Reviews Cancer 5, no. 1 (January 2005): 5. http://dx.doi.org/10.1038/nrc1538.

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11

Potts, Malia B., and Scott Cameron. "Cell lineage and cell death: Caenorhabditis elegans and cancer research." Nature Reviews Cancer 11, no. 1 (December 2, 2010): 50–58. http://dx.doi.org/10.1038/nrc2984.

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12

Kunzelmann, Karl, Jiraporn Ousingsawat, Roberta Benedetto, Ines Cabrita, and Rainer Schreiber. "Contribution of Anoctamins to Cell Survival and Cell Death." Cancers 11, no. 3 (March 19, 2019): 382. http://dx.doi.org/10.3390/cancers11030382.

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Before anoctamins (TMEM16 proteins) were identified as a family of Ca2+-activated chloride channels and phospholipid scramblases, the founding member anoctamin 1 (ANO1, TMEM16A) was known as DOG1, a marker protein for gastrointestinal stromal tumors (GIST). Meanwhile, ANO1 has been examined in more detail, and the role of ANO1 in cell proliferation and the development of different types of malignomas is now well established. While ANO5, ANO7, and ANO9 may also be relevant for growth of cancers, evidence has been provided for a role of ANO6 (TMEM16F) in regulated cell death. The cellular mechanisms by which anoctamins control cell proliferation and cell death, respectively, are just emerging; however, the pronounced effects of anoctamins on intracellular Ca2+ levels are likely to play a significant role. Recent results suggest that some anoctamins control membrane exocytosis by setting Ca2+i levels near the plasma membrane, and/or by controlling the intracellular Cl− concentration. Exocytosis and increased membrane trafficking induced by ANO1 and ANO6 may enhance membrane expression of other chloride channels, such as CFTR and volume activated chloride channels (VRAC). Notably, ANO6-induced phospholipid scrambling with exposure of phosphatidylserine is pivotal for the sheddase function of disintegrin and metalloproteinase (ADAM). This may support cell death and tumorigenic activity of IL-6 by inducing IL-6 trans-signaling. The reported anticancer effects of the anthelminthic drug niclosamide are probably related to the potent inhibitory effect on ANO1, apart from inducing cell cycle arrest through the Let-7d/CDC34 axis. On the contrary, pronounced activation of ANO6 due to a large increase in intracellular calcium, activation of phospholipase A2 or lipid peroxidation, can lead to ferroptotic death of cancer cells. It therefore appears reasonable to search for both inhibitors and potent activators of TMEM16 in order to interfere with cancer growth and metastasis.

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13

Fathima, Samreen, Swati Sinha, and Sainitin Donakonda. "Network Analysis Identifies Drug Targets and Small Molecules to Modulate Apoptosis Resistant Cancers." Cancers 13, no. 4 (February 18, 2021): 851. http://dx.doi.org/10.3390/cancers13040851.

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Programed cell death or apoptosis fails to induce cell death in many recalcitrant cancers. Thus, there is an emerging need to activate the alternate cell death pathways in such cancers. In this study, we analyzed the apoptosis-resistant colon adenocarcinoma, glioblastoma multiforme, and small cell lung cancers transcriptome profiles. We extracted clusters of non-apoptotic cell death genes from each cancer to understand functional networks affected by these genes and their role in the induction of cell death when apoptosis fails. We identified transcription factors regulating cell death genes and protein–protein interaction networks to understand their role in regulating cell death mechanisms. Topological analysis of networks yielded FANCD2 (ferroptosis, negative regulator, down), NCOA4 (ferroptosis, up), IKBKB (alkaliptosis, down), and RHOA (entotic cell death, down) as potential drug targets in colon adenocarcinoma, glioblastoma multiforme, small cell lung cancer phenotypes respectively. We also assessed the miRNA association with the drug targets. We identified tumor growth-related interacting partners based on the pathway information of drug-target interaction networks. The protein–protein interaction binding site between the drug targets and their interacting proteins provided an opportunity to identify small molecules that can modulate the activity of functional cell death interactions in each cancer. Overall, our systematic screening of non-apoptotic cell death-related genes uncovered targets helpful for cancer therapy.

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14

Labi, V., and M. Erlacher. "How cell death shapes cancer." Cell Death & Disease 6, no. 3 (March 2015): e1675-e1675. http://dx.doi.org/10.1038/cddis.2015.20.

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15

Kroemer, Guido. "Cell death and cancer: an introduction." Oncogene 23, no. 16 (April 2004): 2744–45. http://dx.doi.org/10.1038/sj.onc.1207531.

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16

Hofius, Daniel, Dimitrios I. Tsitsigiannis, Jonathan D. G. Jones, and John Mundy. "Inducible cell death in plant immunity." Seminars in Cancer Biology 17, no. 2 (April 2007): 166–87. http://dx.doi.org/10.1016/j.semcancer.2006.12.001.

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17

Özören, Nesrin, and Wafik S. El-Deiry. "Cell surface Death Receptor signaling in normal and cancer cells." Seminars in Cancer Biology 13, no. 2 (April 2003): 135–47. http://dx.doi.org/10.1016/s1044-579x(02)00131-1.

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18

Daido, Shigeru, Takao Kanzawa, Akitsugu Yamamoto, Hayato Takeuchi, Yasuko Kondo, and Seiji Kondo. "Pivotal Role of the Cell Death Factor BNIP3 in Ceramide-Induced Autophagic Cell Death in Malignant Glioma Cells." Cancer Research 64, no. 12 (June 15, 2004): 4286–93. http://dx.doi.org/10.1158/0008-5472.can-03-3084.

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19

Letai, Anthony. "Cell Death and Cancer Therapy: Don't Forget to Kill the Cancer Cell!" Clinical Cancer Research 21, no. 22 (November 12, 2015): 5015–20. http://dx.doi.org/10.1158/1078-0432.ccr-15-1204.

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20

Castelli, Vanessa, Antonio Giordano, Elisabetta Benedetti, Francesco Giansanti, Massimiliano Quintiliani, Annamaria Cimini, and Michele d’Angelo. "The Great Escape: The Power of Cancer Stem Cells to Evade Programmed Cell Death." Cancers 13, no. 2 (January 17, 2021): 328. http://dx.doi.org/10.3390/cancers13020328.

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Cancer is one of the primary causes of death worldwide. Tumour malignancy is related to tumor heterogeneity, which has been suggested to be due to a small subpopulation of tumor cells named cancer stem cells (CSCs). CSCs exert a key role in metastasis development, tumor recurrence, and also epithelial–mesenchymal transition, apoptotic resistance, self-renewal, tumorigenesis, differentiation, and drug resistance. Several current therapies fail to eradicate tumors due to the ability of CSCs to escape different programmed cell deaths. Thus, developing CSC-selective and programmed death-inducing therapeutic approaches appears to be of primary importance. In this review, we discuss the main programmed cell death occurring in cancer and the promising CSC-targeting agents developed in recent years. Even if the reported studies are encouraging, further investigations are necessary to establish a combination of agents able to eradicate CSCs or inhibit their growth and proliferation.

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21

Maniam, Subashani, and Sandra Maniam. "Small Molecules Targeting Programmed Cell Death in Breast Cancer Cells." International Journal of Molecular Sciences 22, no. 18 (September 8, 2021): 9722. http://dx.doi.org/10.3390/ijms22189722.

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Targeted chemotherapy has become the forefront for cancer treatment in recent years. The selective and specific features allow more effective treatment with reduced side effects. Most targeted therapies, which include small molecules, act on specific molecular targets that are altered in tumour cells, mainly in cancers such as breast, lung, colorectal, lymphoma and leukaemia. With the recent exponential progress in drug development, programmed cell death, which includes apoptosis and autophagy, has become a promising therapeutic target. The research in identifying effective small molecules that target compensatory mechanisms in tumour cells alleviates the emergence of drug resistance. Due to the heterogenous nature of breast cancer, various attempts were made to overcome chemoresistance. Amongst breast cancers, triple negative breast cancer (TNBC) is of particular interest due to its heterogeneous nature in response to chemotherapy. TNBC represents approximately 15% of all breast tumours, however, and still has a poor prognosis. Unlike other breast tumours, signature targets lack for TNBCs, causing high morbidity and mortality. This review highlights several small molecules with promising preclinical data that target autophagy and apoptosis to induce cell death in TNBC cells.

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22

McCarthy, Nicola. "The ARTS of cell death." Nature Reviews Cancer 10, no. 12 (November 24, 2010): 816–17. http://dx.doi.org/10.1038/nrc2969.

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23

Kirkwood, TBL. "Cellular Aging and Cell Death." British Journal of Cancer 76, no. 1 (July 1997): 138. http://dx.doi.org/10.1038/bjc.1997.352.

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24

Meyn, Ravmond E., Clifton Stephens, and Luka Milas. "Programmed cell death and radioresistance." Cancer and Metastasis Review 15, no. 1 (March 1996): 119–31. http://dx.doi.org/10.1007/bf00049491.

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25

Hååg, P., M. Lagergren Lindberg, D. Zong, L. Kanter, R. Lewensohn, L. Stenke, and K. Viktorsson. "219 Cytotoxicity and cell death signaling in stem cell like AML cells." European Journal of Cancer Supplements 8, no. 5 (June 2010): 57. http://dx.doi.org/10.1016/s1359-6349(10)71026-0.

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26

Tsuda, Hiroyuki, Ren-Wei Huang, and Kiyoshi Takatsuki. "Interleukin-2 Prevents Programmed Cell Death in Adult T-Cell Leukemia Cells." Japanese Journal of Cancer Research 84, no. 4 (April 1993): 431–37. http://dx.doi.org/10.1111/j.1349-7006.1993.tb00154.x.

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27

Potts, Malia B., and Scott Cameron. "Erratum: Cell lineage and cell death: Caenorhabditis elegans and cancer research." Nature Reviews Cancer 11, no. 4 (March 1, 2011): 309. http://dx.doi.org/10.1038/nrc3041.

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28

Morgan, Ethan L., and Andrew Macdonald. "JAK2 Inhibition Impairs Proliferation and Sensitises Cervical Cancer Cells to Cisplatin-Induced Cell Death." Cancers 11, no. 12 (December 4, 2019): 1934. http://dx.doi.org/10.3390/cancers11121934.

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Persistent infection with high-risk human papillomavirus (HPV) is the underlying cause of ~5% of all human cancers, including the majority of cervical carcinomas and many other ano-genital and oral cancers. A major challenge remains to identify key host targets of HPV and to reveal how they contribute to virus-mediated malignancy. The HPV E6 oncoprotein aberrantly activates the signal transducer and activator of transcription 3 (STAT3) transcription factor and this is achieved by a virus-driven increase in the levels of the pro-inflammatory cytokine interleukin-6 (IL-6) in HPV positive cervical cancers cells. Crucially, STAT3 activity is essential for the proliferation and survival of cervical cancer cells, suggesting that targeting STAT3 may have therapeutic potential. Unfortunately, the development of direct STAT3 inhibitors has been problematic in the clinic due to toxicity issues identified in early stage trials. To overcome this issue, we focused on the protein Janus kinase 2 (JAK2), which phosphorylates STAT3 and is essential for STAT3 activation. Here, we demonstrate that inhibiting JAK2 reduces cell proliferation and induces apoptosis in HPV transformed cervical cancer cells. We further establish that this is due to inhibition of phosphorylation of the JAK2 substrates STAT3 and STAT5. Finally, we demonstrate that the clinically available JAK2 inhibitor Ruxolitinib synergises with cisplatin in inducing apoptosis, highlighting JAK2 as a promising therapeutic target in HPV-driven cancers.

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29

Zappavigna, S., A. Luce, G. Vitale, N. Merola, S. Facchini, and M. Caraglia. "Autophagic cell death: A new frontier in cancer research." Advances in Bioscience and Biotechnology 04, no. 02 (2013): 250–62. http://dx.doi.org/10.4236/abb.2013.42034.

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30

Ahmed, Asma, and Stephen W. G. Tait. "Targeting immunogenic cell death in cancer." Molecular Oncology 14, no. 12 (December 2020): 2994–3006. http://dx.doi.org/10.1002/1878-0261.12851.

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31

Rammer, Paul, Line Groth-Pedersen, Thomas Kirkegaard, Mads Daugaard, Anna Rytter, Piotr Szyniarowski, Maria Høyer-Hansen, et al. "BAMLET Activates a Lysosomal Cell Death Program in Cancer Cells." Molecular Cancer Therapeutics 9, no. 1 (January 2010): 24–32. http://dx.doi.org/10.1158/1535-7163.mct-09-0559.

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32

Lahusen, Tyler J., and Chu-Xia Deng. "SRT1720 Induces Lysosomal-Dependent Cell Death of Breast Cancer Cells." Molecular Cancer Therapeutics 14, no. 1 (November 19, 2014): 183–92. http://dx.doi.org/10.1158/1535-7163.mct-14-0584.

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33

Floryk, Daniel, and Timothy C. Thompson. "Perifosine induces differentiation and cell death in prostate cancer cells." Cancer Letters 266, no. 2 (August 2008): 216–26. http://dx.doi.org/10.1016/j.canlet.2008.02.060.

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34

Benti, Senyi, Purushottam B. Tiwari, Dustin W. Goodlett, Leily Daneshian, Grant B. Kern, Mark D. Smith, Aykut Uren, Maksymilian Chruszcz, Linda S. Shimizu, and Geeta Upadhyay. "Small Molecule Binds with Lymphocyte Antigen 6K to Induce Cancer Cell Death." Cancers 12, no. 2 (February 22, 2020): 509. http://dx.doi.org/10.3390/cancers12020509.

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Elevated gene expression of Lymphocyte antigen 6K (LY6K) in cancer cells is associated with poor survival outcomes in multiple different cancer types including cervical, breast, ovarian, lung, and head and neck cancer. Since inhibition of LY6K expression inhibits cancer cell growth, we set out to explore whether pharmacological inhibition of LY6K could produce the same effect. We screened small molecule libraries for direct binding to recombinant LY6K protein in a surface plasmon resonance assay. We found that NSC243928 directly binds to the full-length and mature forms of LY6K and inhibits growth of HeLa cells that express LY6K. NSC243928 did not display binding with LY6D or LY6E. Our data demonstrate a first-time proof of principle study that pharmacological inhibition of LY6K using small molecules in cancer cells is a valid approach to developing targeted therapies against LY6K. This approach will be specifically relevant in hard-to-treat cancers where LY6K is highly expressed, such as cervical, pancreatic, ovarian, head and neck, lung, gastric, and triple-negative breast cancers.

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35

Kutikov, Alexander, Brian L. Egleston, Yu-Ning Wong, and Robert G. Uzzo. "Evaluating Overall Survival and Competing Risks of Death in Patients With Localized Renal Cell Carcinoma Using a Comprehensive Nomogram." Journal of Clinical Oncology 28, no. 2 (January 10, 2010): 311–17. http://dx.doi.org/10.1200/jco.2009.22.4816.

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Purpose Many patients with localized node-negative renal cell carcinoma (RCC) are elderly with competing comorbidities. Their overall survival benefit after surgical treatment is unknown. We reviewed cases in the Surveillance, Epidemiology, and End Results (SEER) database to evaluate the impact of kidney cancer versus competing causes of death in patients with localized RCC and develop a comprehensive nomogram to quantitate survival differences. Methods We identified individuals with localized, surgically treated clear-cell, papillary, or chromophobe RCC in SEER (1988 through 2003). We used Fine and Gray competing risks proportional hazards regressions to predict 5-year probabilities of three competing mortality outcomes: kidney cancer death, other cancer death, and noncancer death. Results We identified 30,801 cases of localized RCC (median age, 62 years; median tumor size, 4.5 cm). Five-year probabilities of kidney cancer death, other cancer death, and noncancer death were 4%, 7%, and 11%, respectively. Age was strongly predictive of mortality and most predictive of nonkidney cancer deaths (P < .001). Increasing tumor size was related to death from RCC and inversely related to noncancer deaths (P < .001). Racial differences in outcomes were most pronounced for nonkidney cancer deaths (P < .001). Men were more likely to die than women from all causes (P < .002). This nomogram integrates commonly available factors into a useful tool for comparing competing risks of death. Conclusion Management of localized RCC must consider competing causes of mortality, particularly in elderly populations. Effective decision making requires treatment trade-off calculations. We present a tool to quantitate competing causes of mortality in patients with localized RCC.

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36

Tang, Wenwen, Shaomi Zhu, Xin Liang, Chi Liu, and Linjiang Song. "The Crosstalk Between Long Non-Coding RNAs and Various Types of Death in Cancer Cells." Technology in Cancer Research & Treatment 20 (January 1, 2021): 153303382110330. http://dx.doi.org/10.1177/15330338211033044.

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With the increasing aging population, cancer has become one of the leading causes of death worldwide, and the number of cancer cases and deaths is only anticipated to grow further. Long non-coding RNAs (lncRNAs), which are closely associated with the expression level of downstream genes and various types of bioactivity, are regarded as one of the key regulators of cancer cell proliferation and death. Cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, plays a vital role in the progression of cancer. A better understanding of the regulatory relationships between lncRNAs and these various types of cancer cell death is therefore urgently required. The occurrence and development of tumors can be controlled by increasing or decreasing the expression of lncRNAs, a method which confers broad prospects for cancer treatment. Therefore, it is urgent for us to understand the influence of lncRNAs on the development of different modes of tumor death, and to evaluate whether lncRNAs have the potential to be used as biological targets for inducing cell death and predicting prognosis and recurrence of chemotherapy. The purpose of this review is to provide an overview of the various forms of cancer cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, and to describe the mechanisms of different types of cancer cell death that are regulated by lncRNAs in order to explore potential targets for cancer therapy.

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37

Borst, Piet, and Sven Rottenberg. "Cancer cell death by programmed necrosis?" Drug Resistance Updates 7, no. 6 (December 2004): 321–24. http://dx.doi.org/10.1016/j.drup.2004.11.003.

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38

Guicciardi, Maria Eugenia, Marcel Leist, and Gregory J. Gores. "Lysosomes in cell death." Oncogene 23, no. 16 (April 2004): 2881–90. http://dx.doi.org/10.1038/sj.onc.1207512.

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39

Lockshin, Richard A., and Zahra Zakeri. "Caspase-independent cell death?" Oncogene 23, no. 16 (April 2004): 2766–73. http://dx.doi.org/10.1038/sj.onc.1207514.

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40

Essafi, Makram, Alice D. Baudot, Xavier Mouska, Jill-Patrice Cassuto, Michel Ticchioni, and Marcel Deckert. "Cell-Penetrating TAT-FOXO3 Fusion Proteins Induce Apoptotic Cell Death in Leukemic Cells." Molecular Cancer Therapeutics 10, no. 1 (January 2011): 37–46. http://dx.doi.org/10.1158/1535-7163.mct-10-0482.

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41

De Laurenzi, V., D. Barcaroli, M. Ranalli, and G. Melino. "Regulation of p73 in cell death." European Journal of Cancer 37 (April 2001): S7. http://dx.doi.org/10.1016/s0959-8049(01)80514-1.

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42

Kepp, Oliver, Antoine Tesniere, Laurence Zitvogel, and Guido Kroemer. "The immunogenicity of tumor cell death." Current Opinion in Oncology 21, no. 1 (January 2009): 71–76. http://dx.doi.org/10.1097/cco.0b013e32831bc375.

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43

Jäättelä, M., T. Kirkegaard, O. D. Olsen, N. H. T. Pedersen, L. Groth-Pedersen, J. Nylandsted, C. Arenz, C. Ejsing, and J. Knudsen. "38 The lysosomal cell death pathway." European Journal of Cancer Supplements 8, no. 7 (November 2010): 22. http://dx.doi.org/10.1016/s1359-6349(10)71743-2.

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44

Alderton, Gemma K. "Worming your way to cell death." Nature Reviews Cancer 8, no. 11 (November 2008): 830–31. http://dx.doi.org/10.1038/nrc2533.

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45

Murphy, Maureen E. "Regulation of Cell Death in Oncogenesis." Cancer Research 65, no. 18 (September 15, 2005): 8069–71. http://dx.doi.org/10.1158/0008-5472.can-05-2439.

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46

Hsu, Brenda, Maria C. Marin, and Timothy J. McDonnell. "Cell death regulation during multistep lymphomagenesis." Cancer Letters 94, no. 1 (July 1995): 17–23. http://dx.doi.org/10.1016/0304-3835(95)03836-l.

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47

Stevens, Joshua B., Guo Liu, Steven W. Bremer, Karen J. Ye, Wenxin Xu, Jing Xu, Yi Sun, et al. "Mitotic Cell Death by Chromosome Fragmentation." Cancer Research 67, no. 16 (August 15, 2007): 7686–94. http://dx.doi.org/10.1158/0008-5472.can-07-0472.

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48

Bowersox, J. "Sphingolipids Implicated in Programmed Cell Death." JNCI Journal of the National Cancer Institute 85, no. 9 (May 5, 1993): 696–97. http://dx.doi.org/10.1093/jnci/85.9.696.

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49

Benz, E. J., D. G. Nathan, R. K. Amaravadi, and N. N. Danial. "Targeting the Cell Death-Survival Equation." Clinical Cancer Research 13, no. 24 (December 15, 2007): 7250–53. http://dx.doi.org/10.1158/1078-0432.ccr-07-2221.

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50

Zaitceva, Victoria, Gelina S. Kopeina, and Boris Zhivotovsky. "Anastasis: Return Journey from Cell Death." Cancers 13, no. 15 (July 22, 2021): 3671. http://dx.doi.org/10.3390/cancers13153671.

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For over 20 years, it has been a dogma that once the integrity of mitochondria is disrupted and proapoptotic proteins that are normally located in the intermembrane space of mitochondria appeared in the cytoplasm, the process of cell death becomes inevitable. However, it has been recently shown that upon removal of the death signal, even at the stage of disturbance in the mitochondria, cells can recover and continue to grow. This phenomenon was named anastasis. Here, we will critically discuss the present knowledge concerning the mechanisms of cell death reversal, or development of anastasis, methods for its detection, and what role signaling from different intracellular compartments plays in anastasis stimulation.

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