Colorimetric detection of glutathione in cells based on peroxidase-like activity of gold nanoclusters: A promising powerful tool for identifying cancer cells

2017 ◽  
Vol 967 ◽  
pp. 64-69 ◽  
Author(s):  
Jiayu Feng ◽  
Pengcheng Huang ◽  
Shuizhen Shi ◽  
Ke-Yu Deng ◽  
Fang-Ying Wu
Keyword(s):  
Cancer Cells ◽  
Colorimetric Detection ◽  
Gold Nanoclusters ◽  
In Cells

scholarly journals RasOncogene-Mediated Progressive Silencing of Extracellular Superoxide Dismutase in Tumorigenesis

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Francesca Cammarota ◽  
Gabriella de Vita ◽  
Marco Salvatore ◽  
Mikko O. Laukkanen
Keyword(s):  
Superoxide Dismutase ◽  
Cancer Cells ◽  
Self Regulation ◽  
Thyroid Cell ◽  
Extracellular Superoxide Dismutase ◽  
Mrna Synthesis ◽  
Ras Activation ◽  
Degree Of Differentiation ◽  
In Cells

Extracellular superoxide dismutase (SOD3) is a secreted enzyme that uses superoxide anion as a substrate in a dismutase reaction that results in the formation of hydrogen peroxide. Both of these reactive oxygen species affect growth signaling in cells. Although SOD3 has growth-supporting characteristics, the expression ofSOD3is downregulated in epithelial cancer cells. In the current work, we studied the mechanisms regulatingSOD3expressionin vitrousing thyroid cell models representing different stages of thyroid cancer. We demonstrate that a low level of RAS activation increasesSOD3mRNA synthesis that then gradually decreases with increasing levels of RAS activation and the decreasing degree of differentiation of the cancer cells. Our data indicate thatSOD3regulation can be divided into two classes. The first class involves RAS–driven reversible regulation ofSOD3expression that can be mediated by the following mechanisms: RAS GTPase regulatory genes that are responsible forSOD3self-regulation; RAS-stimulated p38 MAPK activation; and RAS-activated increased expression of themir21microRNA, which inversely correlates withsod3mRNA expression. The second class involves permanent silencing ofSOD3mediated by epigenetic DNA methylation in cells that represent more advanced cancers. Therefore, the work suggests thatSOD3belongs to the group ofrasoncogene-silenced genes.

scholarly journals Nuclear envelope rupture is induced by actin-based nucleus confinement

2016 ◽  
Vol 215 (1) ◽  
pp. 27-36 ◽  
Author(s):  
Emily M. Hatch ◽  
Martin W. Hetzer
Keyword(s):  
Nuclear Envelope ◽  
Cancer Cells ◽  
Nuclear Membrane ◽  
Nuclear Lamina ◽  
Membrane Stability ◽  
Linc Complex ◽  
Actin Bundles ◽  
In Cells

Repeated rounds of nuclear envelope (NE) rupture and repair have been observed in laminopathy and cancer cells and result in intermittent loss of nucleus compartmentalization. Currently, the causes of NE rupture are unclear. Here, we show that NE rupture in cancer cells relies on the assembly of contractile actin bundles that interact with the nucleus via the linker of nucleoskeleton and cytoskeleton (LINC) complex. We found that the loss of actin bundles or the LINC complex did not rescue nuclear lamina defects, a previously identified determinant of nuclear membrane stability, but did decrease the number and size of chromatin hernias. Finally, NE rupture inhibition could be rescued in cells treated with actin-depolymerizing drugs by mechanically constraining nucleus height. These data suggest a model of NE rupture where weak membrane areas, caused by defects in lamina organization, rupture because of an increase in intranuclear pressure from actin-based nucleus confinement.

Combined Raman and AFM detection of changes in HeLa cervical cancer cells induced by CeO2 nanoparticles – molecular and morphological perspectives

The Analyst ◽  
2020 ◽  
Vol 145 (11) ◽  
pp. 3983-3995
Author(s):  
Mirjana Miletić ◽  
Sonja Aškrabić ◽  
Jan Rüger ◽  
Borislav Vasić ◽  
Lela Korićanac ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Ceo2 Nanoparticles ◽  
Cervical Cancer Cells ◽  
In Cells

Raman and AFM analyses represent a tool for the evaluation of cytotoxic and anti-proliferative effects in cells induced by CeO2 nanoparticles.

scholarly journals The anti-apoptotic proteins NAF-1 and iASPP interact to drive apoptosis in cancer cells

2019 ◽  
Vol 10 (3) ◽  
pp. 665-673 ◽  
Author(s):  
Anat Iosub-Amir ◽  
Fang Bai ◽  
Yang-Sung Sohn ◽  
Luhua Song ◽  
Sagi Tamir ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Interaction Interface ◽  
Apoptotic Proteins ◽  
In Cells ◽  
Apoptosis In Cancer Cells

We reveal a novel interaction between the two anti-apoptotic proteins iASPP and NAF-1, which are overexpressed in many types of cancer cells, and propose that this interaction is required for apoptosis activation in cancer cells. A peptide derived from the interaction interface inhibits apoptosis in cells.

scholarly journals α5β1 integrin recycling promotes Arp2/3-independent cancer cell invasion via the formin FHOD3

2015 ◽  
Vol 210 (6) ◽  
pp. 1013-1031 ◽  
Author(s):  
Nikki R. Paul ◽  
Jennifer L. Allen ◽  
Anna Chapman ◽  
Maria Morlan-Mairal ◽  
Egor Zindy ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cell Invasion ◽  
Molecular Mechanisms ◽  
Cancer Metastasis ◽  
Cancer Cell Invasion ◽  
Coupling Protein ◽  
Α5β1 Integrin ◽  
In Cells

Invasive migration in 3D extracellular matrix (ECM) is crucial to cancer metastasis, yet little is known of the molecular mechanisms that drive reorganization of the cytoskeleton as cancer cells disseminate in vivo. 2D Rac-driven lamellipodial migration is well understood, but how these features apply to 3D migration is not clear. We find that lamellipodia-like protrusions and retrograde actin flow are indeed observed in cells moving in 3D ECM. However, Rab-coupling protein (RCP)-driven endocytic recycling of α5β1 integrin enhances invasive migration of cancer cells into fibronectin-rich 3D ECM, driven by RhoA and filopodial spike-based protrusions, not lamellipodia. Furthermore, we show that actin spike protrusions are Arp2/3-independent. Dynamic actin spike assembly in cells invading in vitro and in vivo is regulated by Formin homology-2 domain containing 3 (FHOD3), which is activated by RhoA/ROCK, establishing a novel mechanism through which the RCP–α5β1 pathway reprograms the actin cytoskeleton to promote invasive migration and local invasion in vivo.

In Situ Growth of Porous Platinum Nanoparticles on Graphene Oxide for Colorimetric Detection of Cancer Cells

2014 ◽  
Vol 86 (5) ◽  
pp. 2711-2718 ◽  
Author(s):  
Ling-Na Zhang ◽  
Hao-Hua Deng ◽  
Feng-Lin Lin ◽  
Xiong-Wei Xu ◽  
Shao-Huang Weng ◽  
...  
Keyword(s):  
Graphene Oxide ◽  
Cancer Cells ◽  
Platinum Nanoparticles ◽  
Colorimetric Detection ◽  
In Situ Growth

Determination of the activity of telomerase in cancer cells by using BSA-protected gold nanoclusters as a fluorescent probe

2018 ◽  
Vol 185 (3) ◽  
Author(s):  
Yujuan Xu ◽  
Peng Zhang ◽  
Zhen Wang ◽  
Shaoping Lv ◽  
Caifeng Ding
Keyword(s):  
Cancer Cells ◽  
Fluorescent Probe ◽  
Gold Nanoclusters

Quantitative Analysis of Glucose Metabolic Cleavage in Glucose Transporters Overexpressed Cancer Cells by Target-Specific Fluorescent Gold Nanoclusters

2018 ◽  
Vol 90 (6) ◽  
pp. 3974-3980 ◽  
Author(s):  
Tsai-Mu Cheng ◽  
Hsueh-Liang Chu ◽  
Yi-Cheng Lee ◽  
Di-Yan Wang ◽  
Che-Chang Chang ◽  
...  
Keyword(s):  
Quantitative Analysis ◽  
Cancer Cells ◽  
Gold Nanoclusters ◽  
Glucose Transporters

scholarly journals SOX30, a target gene of miR-653-5p, represses the proliferation and invasion of prostate cancer cells through inhibition of Wnt/β-catenin signaling

2019 ◽  
Vol 24 (1) ◽  
Author(s):  
Qiang Fu ◽  
Zhenye Sun ◽  
Fan Yang ◽  
Tianci Mao ◽  
Yanyao Gao ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Target Gene ◽  
Prostate Cancer Cell ◽  
Luciferase Reporter ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Proliferation And Invasion ◽  
In Cells

Abstract Background Sex-determining region Y-box containing gene 30 (SOX30) is a newly identified tumor-associated gene in several types of cancer. However, whether SOX30 is involved in the development and progression of prostate cancer remains unknown. This study investigated the potential role of SOX30 in prostate cancer. Methods Prostate cancer cell lines and a normal prostate epithelial cell line were used for the experiments. The expression of SOX30 was determined using quantitative real-time PCR and western blot analysis. The malignant cellular behaviors of prostate cancer were assessed using the Cell Counting Kit-8, colony formation and Matrigel invasion assays. The miRNA–mRNA interaction was validated using the dual-luciferase reporter assay. Results SOX30 expression was lower in cells of prostate cancer lines than in cells of the normal prostate epithelial line. Its overexpression repressed the proliferation and invasion of prostate cancer cells. SOX30 was identified as a target gene of microRNA-653-5p (miR-653-5p), which is upregulated in prostate cancer tissues. MiR-653-5p overexpression decreased SOX30 expression, while its inhibition increased SOX30 expression in prostate cancer cells. MiR-653-5p inhibition also markedly restricted prostate cancer cell proliferation and invasion. SOX30 overexpression or miR-653-5p inhibition significantly reduced β-catenin expression and downregulated the activation of Wnt/β-catenin signaling. SOX30 knockdown significantly reversed the miR-653-5p inhibition-mediated inhibitory effect on the proliferation, invasion and Wnt/β-catenin signaling in prostate cancer cells. Conclusions These results reveal a tumor suppressive function for SOX30 in prostate cancer and confirmed the gene as a target of miR-653-5p. SOX30 upregulation due to miR-653-5p inhibition restricted the proliferation and invasion of prostate cancer cells, and this was associated with Wnt/β-catenin signaling suppression. These findings highlight the importance of the miR-653-5p–SOX30–Wnt/β-catenin signaling axis in prostate cancer progression.

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