scholarly journals C/EBPβ represses p53 to promote cell survival downstream of DNA damage independent of oncogenic Ras and p19Arf

2008 ◽  
Vol 15 (11) ◽  
pp. 1734-1744 ◽  
Author(s):  
S J Ewing ◽  
S Zhu ◽  
F Zhu ◽  
J S House ◽  
R C Smart
Keyword(s):  
Dna Damage ◽  
Cell Survival ◽  
Oncogenic Ras ◽  
Promote Cell Survival

scholarly journals DNA-PK phosphorylation sites on Oct-1 promote cell survival following DNA damage

Oncogene ◽  
2007 ◽  
Vol 26 (27) ◽  
pp. 3980-3988 ◽  
Author(s):  
C Schild-Poulter ◽  
A Shih ◽  
D Tantin ◽  
N C Yarymowich ◽  
S Soubeyrand ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Survival ◽  
Phosphorylation Sites ◽  
Promote Cell Survival

scholarly journals Persistent DNA damage triggers activation of the integrated stress response to promote cell survival under nutrient restriction

BMC Biology ◽  
2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Elena Clementi ◽  
Larissa Inglin ◽  
Erin Beebe ◽  
Corina Gsell ◽  
Zuzana Garajova ◽  
...  
Keyword(s):  
Dna Damage ◽  
Stress Response ◽  
Cell Survival ◽  
Nutrient Restriction ◽  
Integrated Stress Response ◽  
Promote Cell Survival

scholarly journals The DNA damage inducible lncRNA SCAT7 regulates genomic integrity and topoisomerase 1 turnover in lung adenocarcinoma

NAR Cancer ◽  
2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Luisa Statello ◽  
Mohamad M Ali ◽  
Silke Reischl ◽  
Sagar Mahale ◽  
Subazini Thankaswamy Kosalai ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Cancer Biology ◽  
Topoisomerase I ◽  
Cell Cycle Checkpoints ◽  
Topoisomerase 1 ◽  
Damage Response ◽  
Promote Cell Survival

Abstract Despite the rapid improvements in unveiling the importance of lncRNAs in all aspects of cancer biology, there is still a void in mechanistic understanding of their role in the DNA damage response. Here we explored the potential role of the oncogenic lncRNA SCAT7 (ELF3-AS1) in the maintenance of genome integrity. We show that SCAT7 is upregulated in response to DNA-damaging drugs like cisplatin and camptothecin, where SCAT7 expression is required to promote cell survival. SCAT7 silencing leads to decreased proliferation of cisplatin-resistant cells in vitro and in vivo through interfering with cell cycle checkpoints and DNA repair molecular pathways. SCAT7 regulates ATR signaling, promoting homologous recombination. Importantly, SCAT7 also takes part in proteasome-mediated topoisomerase I (TOP1) degradation, and its depletion causes an accumulation of TOP1–cc structures responsible for the high levels of intrinsic DNA damage. Thus, our data demonstrate that SCAT7 is an important constituent of the DNA damage response pathway and serves as a potential therapeutic target for hard-to-treat drug resistant cancers.

Kinase cascades regulating entry into apoptosis

1997 ◽  
Vol 61 (1) ◽  
pp. 33-46
Author(s):  
P Anderson
Keyword(s):  
Cell Death ◽  
Cell Surface ◽  
Cell Survival ◽  
Tyrosine Kinases ◽  
Uv Light ◽  
Apoptotic Cell ◽  
Paracrine Factors ◽  
Surface Receptors ◽  
Promote Cell Survival ◽  
Necrosis Factor

All cells are constantly exposed to conflicting environment cues that signal cell survival or cell death. Survival signals are delivered by autocrine or paracrine factors that actively suppress a default death pathway. In addition to survival factor withdrawal, cell death can be triggered by environmental stresses such as heat, UV light, and hyperosmolarity or by dedicated death receptors (e.g., FAS/APO-1 and tumor necrosis factor [TNF] receptors) that are counterparts of growth factor or survival receptors at the cell surface. One of the ways that cells integrate conflicting exogenous stimuli is by phosphorylation (or dephosphorylation) of cellular constituents by interacting cascades of serine/threonine and tyrosine protein kinases (and phosphatases). Survival factors (e.g., growth factors and mitogens) activate receptor tyrosine kinases and selected mitogen-activated, cyclin-dependent, lipid-activated, nucleic acid-dependent, and cyclic AMP-dependent kinases to promote cell survival and proliferation, whereas environmental stress (or death factors such as FAS/APO-1 ligand and TNF-alpha) activates different members of these kinase families to inhibit cell growth and, under some circumstances, promote apoptotic cell death. Because individual kinase cascades can interact with one another, they are able to integrate conflicting exogenous stimuli and provide a link between cell surface receptors and the biochemical pathways leading to cell proliferation or cell death.

Oncogenic H-Ras and PI3K signaling can inhibit E-cadherin-dependent apoptosis and promote cell survival after photodynamic therapy in mouse keratinocytes

2009 ◽  
Vol 219 (1) ◽  
pp. 84-93 ◽  
Author(s):  
Jesús Espada ◽  
Sergio Galaz ◽  
Francisco Sanz-Rodríguez ◽  
Alfonso Blázquez-Castro ◽  
Juan Carlos Stockert ◽  
...  
Keyword(s):  
Photodynamic Therapy ◽  
Cell Survival ◽  
Pi3k Signaling ◽  
Promote Cell Survival ◽  
Mouse Keratinocytes ◽  
E Cadherin
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