Biosynthesized Vitis vinifera seed gold nanoparticles induce apoptotic cell death in A431 skin cancer cells

RSC Advances ◽  
2016 ◽  
Vol 6 (85) ◽  
pp. 82205-82218 ◽  
Author(s):  
J. Grace Nirmala ◽  
S. Akila ◽  
M. S. A. Muthukumar Nadar ◽  
R. T. Narendhirakannan ◽  
Suvro Chatterjee
Keyword(s):  
Gold Nanoparticles ◽  
Cell Death ◽  
Skin Cancer ◽  
Vitis Vinifera ◽  
Cancer Cells ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
A431 Cell ◽  
Apoptotic Effects

Cytotoxic and apoptotic effects of Vitis vinifera seed gold nanoparticles on A431 cell lines.

scholarly journals Cytotoxicity and apoptotic cell death induced by Vitis vinifera peel and seed extracts in A431 skin cancer cells

2017 ◽  
Vol 70 (2) ◽  
pp. 537-554 ◽  
Author(s):  
J. Grace Nirmala ◽  
S. Evangeline Celsia ◽  
Akila Swaminathan ◽  
R. T. Narendhirakannan ◽  
Suvro Chatterjee
Keyword(s):  
Cell Death ◽  
Skin Cancer ◽  
Vitis Vinifera ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Seed Extracts

scholarly journals Chitosan-Coated Gold Nanoparticles Induce Low Cytotoxicity and Low ROS Production in Primary Leucocytes, Independent of Their Proliferative Status

Pharmaceutics ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 942
Author(s):  
Helen Yarimet Lorenzo-Anota ◽  
Diana G. Zarate-Triviño ◽  
Jorge Alberto Uribe-Echeverría ◽  
Andrea Ávila-Ávila ◽  
José Raúl Rangel-López ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Cell Death ◽  
Cancer Cells ◽  
Cell Lines ◽  
Mononuclear Cells ◽  
Bone Marrow Cells ◽  
Lymphoid Cells ◽  
Ros Production ◽  
Biomedical Sciences ◽  
Peripheral Blood Mononuclear

(1) Background: Chitosan-coated gold nanoparticles (CH-AuNPs) have important theranostic applications in biomedical sciences, including cancer research. However, although cell cytotoxicity has been studied in cancerous cells, little is known about their effect in proliferating primary leukocytes. Here, we assessed the effect of CH-AuNPs and the implication of ROS on non-cancerous endothelial and fibroblast cell lines and in proliferative lymphoid cells. (2) Methods: The Turkevich method was used to synthetize gold nanoparticles. We tested cell viability, cell death, ROS production, and cell cycle in primary lymphoid cells, compared with non-cancer and cancer cell lines. Concanavalin A (ConA) or lipopolysaccharide (LPS) were used to induce proliferation on lymphoid cells. (3) Results: CH-AuNPs presented high cytotoxicity and ROS production against cancer cells compared to non-cancer cells; they also induced a different pattern of ROS production in peripheral blood mononuclear cells (PBMCs). No significant cell-death difference was found in PBMCs, splenic mononuclear cells, and bone marrow cells (BMC) with or without a proliferative stimuli. (4) Conclusions: Taken together, our results highlight the selectivity of CH-AuNPs to cancer cells, discarding a consistent cytotoxicity upon proliferative cells including endothelial, fibroblast, and lymphoid cells, and suggest their application in cancer treatment without affecting immune cells.

scholarly journals Quinacrine-Induced Autophagy in Ovarian Cancer Triggers Cathepsin-L Mediated Lysosomal/Mitochondrial Membrane Permeabilization and Cell Death

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2004
Author(s):  
Prabhu Thirusangu ◽  
Christopher L. Pathoulas ◽  
Upasana Ray ◽  
Yinan Xiao ◽  
Julie Staub ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Death ◽  
Cytochrome C ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Cathepsin L ◽  
Membrane Permeabilization ◽  
Apoptotic Cell Death ◽  
Ovarian Cancer Cells ◽  
Autophagic Flux

We previously reported that the antimalarial compound quinacrine (QC) induces autophagy in ovarian cancer cells. In the current study, we uncovered that QC significantly upregulates cathepsin L (CTSL) but not cathepsin B and D levels, implicating the specific role of CTSL in promoting QC-induced autophagic flux and apoptotic cell death in OC cells. Using a Magic Red® cathepsin L activity assay and LysoTracker red, we discerned that QC-induced CTSL activation promotes lysosomal membrane permeability (LMP) resulting in the release of active CTSL into the cytosol to promote apoptotic cell death. We found that QC-induced LMP and CTSL activation promotes Bid cleavage, mitochondrial outer membrane permeabilization (MOMP), and mitochondrial cytochrome-c release. Genetic (shRNA) and pharmacological (Z-FY(tBU)-DMK) inhibition of CTSL markedly reduces QC-induced autophagy, LMP, MOMP, apoptosis, and cell death; whereas induced overexpression of CTSL in ovarian cancer cell lines has an opposite effect. Using recombinant CTSL, we identified p62/SQSTM1 as a novel substrate of CTSL, suggesting that CTSL promotes QC-induced autophagic flux. CTSL activation is specific to QC-induced autophagy since no CTSL activation is seen in ATG5 knockout cells or with the anti-malarial autophagy-inhibiting drug chloroquine. Importantly, we showed that upregulation of CTSL in QC-treated HeyA8MDR xenografts corresponds with attenuation of p62, upregulation of LC3BII, cytochrome-c, tBid, cleaved PARP, and caspase3. Taken together, the data suggest that QC-induced autophagy and CTSL upregulation promote a positive feedback loop leading to excessive autophagic flux, LMP, and MOMP to promote QC-induced cell death in ovarian cancer cells.

scholarly journals Ceramide metabolism regulates autophagy and apoptotic cell death induced by melatonin in liver cancer cells

2015 ◽  
Vol 59 (2) ◽  
pp. 178-189 ◽  
Author(s):  
Raquel Ordoñez ◽  
Anna Fernández ◽  
Néstor Prieto-Domínguez ◽  
Laura Martínez ◽  
Carmen García-Ruiz ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Liver Cancer Cells

scholarly journals Inhibition of Replication Induces Non-Apoptotic Cell Death in Fibroblast Cell Lines Derived from LEC Rats

2003 ◽  
Vol 65 (2) ◽  
pp. 249-254 ◽  
Author(s):  
Masanobu HAYASHI ◽  
Taku HAMASU ◽  
Daiji ENDOH ◽  
Reiko SHIMOJIMA ◽  
Toyo OKUI
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Fibroblast Cell ◽  
Apoptotic Cell Death ◽  
Lec Rats ◽  
Fibroblast Cell Lines

Sulindac induces apoptotic cell death in susceptible human breast cancer cells through, at least in part, inhibition of IKKβ

APOPTOSIS ◽  
2009 ◽  
Vol 14 (7) ◽  
pp. 913-922 ◽  
Author(s):  
A-Mi Seo ◽  
Seung-Woo Hong ◽  
Jae-Sik Shin ◽  
In-Chul Park ◽  
Nam-Joo Hong ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Human Breast Cancer Cells ◽  
Human Breast

scholarly journals ADP-Ribosylation of Actin by the Clostridium botulinum C2 Toxin in Mammalian Cells Results in Delayed Caspase-Dependent Apoptotic Cell Death

2008 ◽  
Vol 76 (10) ◽  
pp. 4600-4608 ◽  
Author(s):  
Karin Heine ◽  
Sascha Pust ◽  
Stefanie Enzenmüller ◽  
Holger Barth
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Mammalian Cells ◽  
Clostridium Botulinum ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Adp Ribosylation ◽  
Mammalian Cell Lines ◽  
Adp Ribosyltransferase ◽  
C2 Toxin

ABSTRACT The binary C2 toxin from Clostridium botulinum mono-ADP-ribosylates G-actin in the cytosol of eukaryotic cells. This modification leads to depolymerization of actin filaments accompanied by cell rounding within 3 h of incubation but does not immediately induce cell death. Here we investigated the long-term responses of mammalian cell lines (HeLa and Vero) following C2 toxin treatment. Cells stayed round even though the toxin was removed from the medium after its internalization into the cells. No unmodified actin reappeared in the C2 toxin-treated cells within 48 h. Despite actin being completely ADP-ribosylated after about 7 h, no obvious decrease in the overall amount of actin was observed for at least 48 h. Therefore, ADP-ribosylation was not a signal for an accelerated degradation of actin in the tested cell lines. C2 toxin treatment resulted in delayed apoptotic cell death that became detectable about 15 to 24 h after toxin application in a portion of the cells. Poly(ADP)-ribosyltransferase 1 (PARP-1) was cleaved in C2 toxin-treated cells, an indication of caspase 3 activation and a hallmark of apoptosis. Furthermore, specific caspase inhibitors prevented C2 toxin-induced apoptosis, implying that caspases 8 and 9 were activated in C2 toxin-treated cells. C2I, the ADP-ribosyltransferase component of the C2 toxin, remained active in the cytosol for at least 48 h, and no extensive degradation of C2I was observed. From our data, we conclude that the long-lived nature of C2I in the host cell cytosol was essential for the nonreversible cytotoxic effect of C2 toxin, resulting in delayed apoptosis of the tested mammalian cells.

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