scholarly journals Altered glycosylation of several metastasis-associated glycoproteins with terminal GalNAc defines the highly invasive cancer cell phenotype

Oncotarget ◽  
2021 ◽  
Author(s):  
Elham Khosrowabadi ◽  
Tomasz Wenta ◽  
Salla Keskitalo ◽  
Aki Manninen ◽  
Sakari Kellokumpu
2019 ◽  
Vol 34 (1) ◽  
Author(s):  
Martin Lamač ◽  
Michal Horáček ◽  
Lucie Červenková Šťastná ◽  
Jindřich Karban ◽  
Lucia Sommerová ◽  
...  

Tumor Biology ◽  
2015 ◽  
Vol 37 (2) ◽  
pp. 2555-2563 ◽  
Author(s):  
Xianglan Zhang ◽  
Im-hee Jung ◽  
Young Sun Hwang

2016 ◽  
Vol 8 (11) ◽  
pp. 1183-1193 ◽  
Author(s):  
Elaheh Alizadeh ◽  
Samanthe Merrick Lyons ◽  
Jordan Marie Castle ◽  
Ashok Prasad

Cancer cells show similar changes in two dimensional cell shape analyzed using Zernike moments.


Genes ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1460
Author(s):  
Wei Zheng ◽  
Luisa Tasselli ◽  
Tie-mei Li ◽  
Katrin F. Chua

The modulation of dynamic histone acetylation states is key for organizing chromatin structure and modulating gene expression and is regulated by histone acetyltransferase (HAT) and histone deacetylase (HDAC) enzymes. The mammalian SIRT6 protein, a member of the Class III HDAC Sirtuin family of NAD+-dependent enzymes, plays pivotal roles in aging, metabolism, and cancer biology. Through its site-specific histone deacetylation activity, SIRT6 promotes chromatin silencing and transcriptional regulation of aging-associated, metabolic, and tumor suppressive gene expression programs. ATP citrate lyase (ACLY) is a nucleo-cytoplasmic enzyme that produces acetyl coenzyme A (acetyl-CoA), which is the required acetyl donor for lysine acetylation by HATs. In addition to playing a central role in generating cytosolic acetyl-CoA for de novo lipogenesis, a growing body of work indicates that ACLY also functions in the nucleus where it contributes to the nutrient-sensitive regulation of nuclear acetyl-CoA availability for histone acetylation in cancer cells. In this study, we have identified a novel function of SIRT6 in controlling nuclear levels of ACLY and ACLY-dependent tumor suppressive gene regulation. The inactivation of SIRT6 in cancer cells leads to the accumulation of nuclear ACLY protein and increases nuclear acetyl-CoA pools, which in turn drive locus-specific histone acetylation and the expression of cancer cell adhesion and migration genes that promote tumor invasiveness. Our findings uncover a novel mechanism of SIRT6 in suppressing invasive cancer cell phenotypes and identify acetyl-CoA responsive cell migration and adhesion genes as downstream targets of SIRT6.


2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Wei Xin Cai ◽  
Li Wu Zheng ◽  
Li Ma ◽  
Hong Zhang Huang ◽  
Ru Qing Yu ◽  
...  

Tumorigenicity and metastatic activity can be visually monitored in cancer cells that were labelled with stable fluorescence. The aim was to establish and validate local and distant spread of subcutaneously previously injected fluorescence transduced human tongue cancer cell lines of epithelial and mesenchymal phenotype in nude mice. A total of 32 four-week-old male athymic Balb/c nude mice were randomly allocated into 4 groups (n=8). A single dose of 0.3 mL PBS containing 1 × 107 of four different cancer cell-lines (UM1, UM1-GFP, UM2, and UM2-RFP) was injected subcutaneously into the right side of their posterolateral back. Validity assessment of the labelled cancer cells’ tumorigenicity was assessed by physical examination, imaging, and histology four weeks after the injection. The tumor take rate of cancer cells was similar in animals injected with either parental or transduced cancer cells. Transduced cancer cells in mice were easily detectable in vivo and after cryosection using fluorescent imaging. UM1 cells showed increased tumor take rate and mean tumor volume, presenting with disorganized histopathological patterns. Fluorescence labelled epithelial and mesenchymal human tongue cancer cell lines do not change in tumorigenicity or cell phenotype after injection in vivo.


FEBS Journal ◽  
2015 ◽  
Vol 283 (1) ◽  
pp. 54-73 ◽  
Author(s):  
Rafael Moreno-Sánchez ◽  
Emma Saavedra ◽  
Juan Carlos Gallardo-Pérez ◽  
Franklin D. Rumjanek ◽  
Sara Rodríguez-Enríquez
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