Erratum: Anastasis: Recovery from the brink of cell death (Royal Society Open Science (2018) 5 (181629)DOI: 10.1098/rsos.180442)

Ho Man Tang, Ho Lam Tang

Research output: Contribution to journalComment/debate

Abstract

In Section 3.2, fourth paragraph, third sentence should read: 'Remarkably, cultured cells have been shown to tolerate sublethal caspase activity without triggering apoptosis [31,128-130].' In Section 3.2, fourth paragraph, third last sentence should read: 'Transcription is also active during anastasis [21,29,32], and that can generate building blocks for the recovering cells to repair damage and regain normal morphology.' In Section 3.3, third paragraph, first sentence should read: 'DNA damage and oncogenic transformation can also be promoted by iMOMP and sublethal activation of caspase-3, presumably through apoptotic DNases, whereas suppressing caspase activation or apoptotic DNase activity has the opposite effect of inhibiting transformation [27,31].' In Section 4, fourth paragraph, third sentence should read: 'Whole-genome gene expression studies have been performed on anastasis in mouse primary liver cells [29] and human cervical cancer HeLa cells [32] after ethanol-induced apoptosis, as well as in mouse NIH3T3 fibroblasts after RIPK3-activated biosensor-induced necroptosis [36], but the putative master regulators of the process remain elusive.' In Section 5, third paragraph, sixth sentence should read: 'Anastasis has been observed in various cultured human cancer cell lines including cervical cancer, small cell lung carcinoma, neuroblastoma, skin cancer, testicular cancer, liver cancer, breast cancer and prostate cancer [21,26,28-30,32,33,85], thereby suggesting that this process could be a common occurrence in cancers'.

Original languageEnglish (US)
Article number181629
JournalRoyal Society Open Science
Volume5
Issue number10
DOIs
StatePublished - Oct 1 2018

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Deoxyribonucleases
Liver Neoplasms
Caspases
Uterine Cervical Neoplasms
Prostatic Neoplasms
Cell Death
Apoptosis
Breast Neoplasms
Small Cell Lung Carcinoma
Testicular Neoplasms
Biosensing Techniques
Skin Neoplasms
Neuroblastoma
HeLa Cells
Caspase 3
DNA Damage
Cultured Cells
Neoplasms
Ethanol
Fibroblasts

ASJC Scopus subject areas

  • General

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Erratum : Anastasis: Recovery from the brink of cell death (Royal Society Open Science (2018) 5 (181629)DOI: 10.1098/rsos.180442). / Tang, Ho Man; Tang, Ho Lam.

In: Royal Society Open Science, Vol. 5, No. 10, 181629, 01.10.2018.

Research output: Contribution to journalComment/debate

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abstract = "In Section 3.2, fourth paragraph, third sentence should read: 'Remarkably, cultured cells have been shown to tolerate sublethal caspase activity without triggering apoptosis [31,128-130].' In Section 3.2, fourth paragraph, third last sentence should read: 'Transcription is also active during anastasis [21,29,32], and that can generate building blocks for the recovering cells to repair damage and regain normal morphology.' In Section 3.3, third paragraph, first sentence should read: 'DNA damage and oncogenic transformation can also be promoted by iMOMP and sublethal activation of caspase-3, presumably through apoptotic DNases, whereas suppressing caspase activation or apoptotic DNase activity has the opposite effect of inhibiting transformation [27,31].' In Section 4, fourth paragraph, third sentence should read: 'Whole-genome gene expression studies have been performed on anastasis in mouse primary liver cells [29] and human cervical cancer HeLa cells [32] after ethanol-induced apoptosis, as well as in mouse NIH3T3 fibroblasts after RIPK3-activated biosensor-induced necroptosis [36], but the putative master regulators of the process remain elusive.' In Section 5, third paragraph, sixth sentence should read: 'Anastasis has been observed in various cultured human cancer cell lines including cervical cancer, small cell lung carcinoma, neuroblastoma, skin cancer, testicular cancer, liver cancer, breast cancer and prostate cancer [21,26,28-30,32,33,85], thereby suggesting that this process could be a common occurrence in cancers'.",
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