scholarly journals A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development

Cancer Cell ◽  
2017 ◽  
Vol 32 (3) ◽  
pp. 342-359.e10 ◽  
Author(s):  
Yannick Boege ◽  
Mohsen Malehmir ◽  
Marc E. Healy ◽  
Kira Bettermann ◽  
Anna Lorentzen ◽  
...  
Keyword(s):  
Dna Damage ◽  
Liver Cancer ◽  
Dual Role ◽  
Cancer Development ◽  
Caspase 8

Dual role of cadmium in rat liver: inducing liver injury and inhibiting the progression of early liver cancer

2021 ◽  
Author(s):  
Honglong Zhang ◽  
Jun Yan ◽  
Ye Xie ◽  
Xuhong Chang ◽  
Junliang Li ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Cancer ◽  
Rat Liver ◽  
Dual Role

scholarly journals A dual role of Cdk2 in DNA damage response

Cell Division ◽  
2009 ◽  
Vol 4 (1) ◽  
pp. 9 ◽  
Author(s):  
Ande Satyanarayana ◽  
Philipp Kaldis
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Dual Role ◽  
Damage Response

Dual role of vitamin C in an oxygen-sensitive system: Discrepancy between DNA damage and dell death

2005 ◽  
Vol 39 (2) ◽  
pp. 213-220 ◽  
Author(s):  
Minyi Shi ◽  
Baohui Xu ◽  
Kazuko Azakami ◽  
Tomohiro Morikawa ◽  
Kunitomo Watanabe ◽  
...  
Keyword(s):  
Dna Damage ◽  
Vitamin C ◽  
Dual Role ◽  
Oxygen Sensitive

Abstract 1880: Role of fatty acid synthase and do novo lipogenesis in liver cancer development in mice.

2013 ◽  
Author(s):  
Xin Chen ◽  
Lei Li ◽  
Chunmei Wang ◽  
Matthias Evert ◽  
Diego F. Calvisi ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Cancer ◽  
Fatty Acid Synthase ◽  
Cancer Development

scholarly journals The dual role of filamin A in cancer: can't live with (too much of) it, can't live without it

2013 ◽  
Vol 20 (6) ◽  
pp. R341-R356 ◽  
Author(s):  
Rosalinda M Savoy ◽  
Paramita M Ghosh
Keyword(s):  
Tumor Formation ◽  
Dual Role ◽  
Cancer Development ◽  
Vascular Endothelial ◽  
Filamin A ◽  
Invasion And Metastasis ◽  
Promoting Effect ◽  
Metastasis Development ◽  
Endothelial Growth Factor

Filamin A (FlnA) has been associated with actin as cytoskeleton regulator. Recently its role in the cell has come under scrutiny for FlnA's involvement in cancer development. FlnA was originally revealed as a cancer-promoting protein, involved in invasion and metastasis. However, recent studies have also found that under certain conditions, it prevented tumor formation or progression, confusing the precise function of FlnA in cancer development. Here, we try to decipher the role of FlnA in cancer and the implications for its dual role. We propose that differences in subcellular localization of FlnA dictate its role in cancer development. In the cytoplasm, FlnA functions in various growth signaling pathways, such as vascular endothelial growth factor, in addition to being involved in cell migration and adhesion pathways, such as R-Ras and integrin signaling. Involvement in these pathways and various others has shown a correlation between high cytoplasmic FlnA levels and invasive cancers. However, an active cleaved form of FlnA can localize to the nucleus rather than the cytoplasm and its interaction with transcription factors has been linked to a decrease in invasiveness of cancers. Therefore, overexpression of FlnA has a tumor-promoting effect, only when it is localized to the cytoplasm, whereas if FlnA undergoes proteolysis and the resulting C-terminal fragment localizes to the nucleus, it acts to suppress tumor growth and inhibit metastasis. Development of drugs to target FlnA and cause cleavage and subsequent localization to the nucleus could be a new and potent field of research in treating cancer.

scholarly journals DNA damage responses and p53 in the aging process

Blood ◽  
2018 ◽  
Vol 131 (5) ◽  
pp. 488-495 ◽  
Author(s):  
Hui-Ling Ou ◽  
Björn Schumacher
Keyword(s):  
Dna Damage ◽  
Aging Process ◽  
Tumor Development ◽  
Cancer Development ◽  
Adaptive Responses ◽  
Genome Maintenance ◽  
Age Related ◽  
Progeroid Syndromes ◽  
Process Studies

Abstract The genome is constantly attacked by genotoxic insults. DNA damage has long been established as a cause of cancer development through its mutagenic consequences. Conversely, radiation therapy and chemotherapy induce DNA damage to drive cells into apoptosis or senescence as outcomes of the DNA damage response (DDR). More recently, DNA damage has been recognized as a causal factor for the aging process. The role of DNA damage in aging and age-related diseases is illustrated by numerous congenital progeroid syndromes that are caused by mutations in genome maintenance pathways. During the past 2 decades, understanding how DDR drives cancer development and contributes to the aging process has progressed rapidly. It turns out that the DDR factor p53 takes center stage during tumor development and also plays an important role in the aging process. Studies in metazoan models ranging from Caenorhabditis elegans to mammals have revealed cell-autonomous and systemic DDR mechanisms that orchestrate adaptive responses that augment maintenance of the aging organism amid gradually accumulating DNA damage.

Sign in / Sign up

Export Citation Format

Share Document