Micromolar taxol, with or without hyperthermia, induces mitotic catastrophe and cell necrosis in HeLa cells

Titanium dioxide nanoparticles (nano-TiO2), as a common nanomaterial, are widely used in water purification, paint, skincare and sunscreens. Its safety has always been a concern. Prior studies have shown that ultraviolet A (UVA) can exacerbate the toxicity of nano-TiO2, including inducing cell apoptosis, changing glycosylation levels, arresting cell cycle, inhibiting tumor cell and bacterial growth. However, whether the combination of UVA and nano-TiO2 cause cell necrosis and its mechanism are still rarely reported. In this study, we investigated the cytotoxicity and phototoxicity of mixture crystalline nano-TiO2 (25% rutile and 75% anatase, 21 nm) under UVA irradiation in HeLa cells. Our results showed that the abnormal membrane integrity and the ultrastructure of HeLa cells, together with the decreased viability induced by nano-TiO2 under UVA irradiation, were due to cell necrosis rather than caspase-dependent apoptosis. Furthermore, nano-TiO2 and UVA generated the reactive oxygen species (ROS) and caused the mitochondrial permeability transition pore (mPTP) of HeLa cells to abnormally open. Cell viability was significantly increased after adding vitamin C (VC) or cyclosporin A (CsA) individually to inhibit ROS and mPTP. Clearance of ROS could not only impede the opening of mPTP but also reduce the rate of cell necrosis. The results suggest the possible mechanism of HeLa cell necrosis caused by nano-TiO2 under UVA irradiation through the ROS-mPTP pathway.

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High LET Radiation Enhances Nocodazole Induced Cell Death in HeLa Cells through Mitotic Catastrophe and Apoptosis

Journal of Radiation Research ◽

10.1269/jrr.10186 ◽

2011 ◽

Vol 52 (4) ◽

pp. 481-489 ◽

Cited By ~ 6

Author(s):

Ping LI ◽

Libin ZHOU ◽

Zhongying DAI ◽

Xiaodong JIN ◽

Xinguo LIU ◽

...

Keyword(s):

Cell Death ◽

Hela Cells ◽

Mitotic Catastrophe ◽

High Let Radiation ◽

High Let

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WEE1 inhibition enhances sensitivity to hypoxia/reoxygenation in HeLa cells

Journal of Radiation Research ◽

10.1093/jrr/rrz045 ◽

2019 ◽

Vol 60 (5) ◽

pp. 709-713

Author(s):

Tatsuaki Goto ◽

Hisao Homma ◽

Atsushi Kaida ◽

Masahiko Miura

Keyword(s):

Hela Cells ◽

Clonogenic Survival ◽

Strand Break ◽

Mitotic Catastrophe ◽

G2 Arrest ◽

Focus Formation ◽

Dna Double Strand Break ◽

M Phase ◽

Colony Forming Assay ◽

Hypoxia Reoxygenation

Abstract Hypoxia/reoxygenation (H/R) treatment reportedly induces DNA damage response (DDR), including DNA double-strand break (DSB) repair and G2 arrest, resulting in reduction of clonogenic survival. Because WEE1 plays a key role in the G2/M checkpoint along with CHK1/2, we investigated the effect of WEE1 inhibition on H/R-induced DDR using HeLa cells. The H/R treatment combined with WEE1 inhibitor abrogated G2 arrest, subsequently leading to the cells entering the M phase, and finally resulting in mitotic catastrophe after prolonged mitosis. Colony-forming assay showed an enhanced decrease in the surviving fraction and the focus formation of BRCA1 was significantly reduced. We demonstrate for the first time that WEE1 inhibition enhances H/R-induced cell death accompanied by mitotic catastrophe and that the process may be mediated by homologous recombination.

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Anti-Cancer Activity of a 5-Aminopyrazole Derivative Lead Compound (BC-7) and Potential Synergistic Cytotoxicity with Cisplatin against Human Cervical Cancer Cells

International Journal of Molecular Sciences ◽

10.3390/ijms20225559 ◽

2019 ◽

Vol 20 (22) ◽

pp. 5559 ◽

Cited By ~ 3

Author(s):

Bresler Swanepoel ◽

George Mihai Nitulescu ◽

Octavian Tudorel Olaru ◽

Luanne Venables ◽

Maryna van de Venter

Keyword(s):

Drug Resistance ◽

Hela Cells ◽

Cytotoxic Effect ◽

Chemotherapeutic Agents ◽

Mitotic Catastrophe ◽

Dependent Manner ◽

Normal Tissues ◽

Synergistic Cytotoxicity ◽

Anti Cancer ◽

Induced Apoptosis

The use of some very well-known chemotherapeutic agents, such as cisplatin, is limited by toxicity in normal tissues and the development of drug resistance. In order to address drug resistance and the side-effects of anti-cancer agents, recent research has focused on finding novel combinations of anti-cancer agents with non-overlapping mechanisms of action. The cytotoxic effect of the synthetic 5-aminopyrazole derivative N-[[3-(4-bromophenyl)-1H-pyrazol-5-yl]-carbamothioyl]-4-chloro-benzamide (BC-7) was evaluated by the bis-Benzamide H 33342 trihydrochloride/propidium iodide (Hoechst 33342/PI) dual staining method against HeLa, MeWo, HepG2, Vero, and MRHF cell lines. Quantitative fluorescence image analysis was used for the elucidation of mechanism of action and synergism with cisplatin in HeLa cells. BC-7 displayed selective cytotoxicity towards HeLa cells (IC50 65.58 ± 8.40 μM) and induced apoptosis in a mitochondrial- and caspase dependent manner. This was most likely preceded by cell cycle arrest in the early M phase and the onset of mitotic catastrophe. BC-7 increased the cytotoxic effect of cisplatin in a synergistic manner with combination index (CI) values less than 0.9 accompanied by highly favourable dose reduction indices. Therefore, the results obtained support the implication that BC-7 has potential anti-cancer properties and that combinations of BC-7 with cisplatin should be further investigated for potential clinical applications.

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Gallic acid induces mitotic catastrophe and inhibits centrosomal clustering in HeLa cells

Toxicology in Vitro ◽

10.1016/j.tiv.2015.09.011 ◽

2015 ◽

Vol 30 (1) ◽

pp. 506-513 ◽

Cited By ~ 12

Author(s):

Si Tan ◽

Xin Guan ◽

Christoph Grün ◽

Zhiqin Zhou ◽

Ute Schepers ◽

...

Keyword(s):

Gallic Acid ◽

Hela Cells ◽

Mitotic Catastrophe

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Normal Cells, but Not Cancer Cells, Survive Severe Plk1 Depletion

Molecular and Cellular Biology ◽

10.1128/mcb.26.6.2093-2108.2006 ◽

2006 ◽

Vol 26 (6) ◽

pp. 2093-2108 ◽

Cited By ~ 221

Author(s):

Xiaoqi Liu ◽

Ming Lei ◽

Raymond L. Erikson

Keyword(s):

Cancer Cells ◽

Hela Cells ◽

Mitotic Catastrophe ◽

Cycle Arrest ◽

Medium Level ◽

Induced Apoptosis ◽

Mcf10a Cells ◽

Therapy Target ◽

High Degree

ABSTRACT We previously reported the phenotype of depletion of polo-like kinase 1 (Plk1) using RNA interference (RNAi) and showed that p53 is stabilized in Plk1-depleted cancer cells. In this study, we further analyzed the Plk1 depletion-induced phenotype in both cancer cells and primary cells. The vector-based RNAi approach was used to evaluate the role of the p53 pathway in Plk1 depletion-induced apoptosis in cancer cells with different p53 backgrounds. Although DNA damage and cell death can occur independently of p53, p53-deficient cancer cells were much more sensitive to Plk1 depletion than cancer cells with functional p53. Next, the lentivirus-based RNAi approach was used to generate a series of Plk1 hypomorphs. In HeLa cells, two weak hypomorphs showed only slight G2/M arrest, a medium hypomorph arrested with 4N DNA content, followed later by apoptosis, and a strong Plk1 hypomorph underwent serious mitotic catastrophe. In well-synchronized HeLa cells, a medium level of Plk1 depletion caused a 2-h delay of mitotic progression, and a high degree of Plk1 depletion significantly delayed mitotic entry and completely blocked cells at mitosis. In striking contrast, normal hTERT-RPE1 and MCF10A cells were much less sensitive to Plk1 depletion than HeLa cells; no apparent cell proliferation defect or cell cycle arrest was observed after Plk1 depletion in these cells. Therefore, these data further support suggestions that Plk1 may be a feasible cancer therapy target.

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Mitotic catastrophe induced in HeLa cells by photodynamic treatment with Zn(II)-phthalocyanine

International Journal of Oncology ◽

10.3892/ijo_32_6_1189 ◽

1992 ◽

Vol 32 (6) ◽

pp. 1189-1196 ◽

Cited By ~ 28

Author(s):

Santiago Rello-Varona

Keyword(s):

Hela Cells ◽

Mitotic Catastrophe ◽

Photodynamic Treatment

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Platinum Compounds as Stains for Electron Microscopy

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100051165 ◽

1974 ◽

Vol 32 ◽

pp. 230-231

Author(s):

S. K. Aggarwal ◽

P. McAllister ◽

R. W. Wagner ◽

B. Rosenberg

Keyword(s):

Electron Microscopy ◽

Hela Cells ◽

Uranyl Acetate ◽

Sarcoma 180 ◽

Platinum Compounds ◽

Kb Cells ◽

En Bloc ◽

Human Lymphoma ◽

Ultrathin Sections ◽

Blue Coloration

Uranyl acetate has been used as an electron stain for en bloc staining as well as for staining ultrathin sections in conjunction with various lead stains (Fig. 1). Present studies reveal that various platinum compounds also show promise as electron stains. Certain platinum compounds have been shown to be effective anti-tumor agents. Of particular interest are the compounds with either uracil or thymine as one of the ligands (cis-Pt(II)-uracil; cis-Pt(II)-thymine). These compounds are amorphous, highly soluble in water and often exhibit an intense blue coloration. These compounds show enough electron density to be used as stains for electron microscopy. Most of the studies are based on various cell lines (human AV, cells, human lymphoma cells, KB cells, Sarcoma-180 ascites cells, chick fibroblasts and HeLa cells) while studies on tissue blocks are in progress.

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