Tetrazolium Violet Induced Apoptosis and Cell Cycle Arrest in Human Lung Cancer A549 Cells

Zhang, Xiao­hong; Zhang, Nan; Lu, Jianmei; Kong, Qingzhong; Zhao, Yunfeng

doi:10.4062/biomolther.2012.20.2.177

Cited by 5 publications

(4 citation statements)

References 31 publications

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“…Apoptosis is mediated by two main pathways, the death receptor pathway (extrinsic) and the mitochondrial pathway (intrinsic). Most anticancer agents exert their cytotoxic effects by inducing apoptosis in tumor cells [3,4]. Therefore, apoptosis induction is vital for successful cancer treatment, and several chemotherapeutic drugs are known to induce apoptosis in vitro [5].…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic Effect of Clerosterol Isolated from Codium fragile on A2058 Human Melanoma Cells

et al. 2013

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The cytotoxic effects and mechanism of action of clerosterol, isolated from the marine alga Codium fragile, were investigated in A2058 human melanoma cells. Clerosterol inhibited the growth of A2058 cells with an IC50 of 150 µM and induced apoptotic cell death, as evidenced by DNA fragmentation, an increase in the number of sub-G1 hypodiploid cells and the presence of apoptotic bodies. Clerosterol treatment caused the loss of mitochondrial membrane potential. Alterations in the expression of apoptosis-associated proteins in response to clerosterol treatment included upregulation of Bax, downregulation of Bcl-2 and activation of caspases 3 and 9. The pan-caspase inhibitor treatment attenuated the expression of the active form of caspases and cell death induced by clerosterol. The present results show that clerosterol exerts its cytotoxic effect in A2058 human melanoma cells by caspases-dependent apoptosis.

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Section: Introductionmentioning

confidence: 99%

Cytotoxic Effect of Clerosterol Isolated from Codium fragile on A2058 Human Melanoma Cells

et al. 2013

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“…The nuclei do not show marked signs of apoptotic fragmentation, blebbing, shrinkage, fragmentation or chromatin condensation [ 67 ] suggesting that this phenotype reflects decreased G 0 /G 1 transition, perhaps paralleled with an increased S and G 2 /M phase dynamics. Rarely also fragmentation signs are seen around the cell nuclei [ 68 ]. The increase in cell/nulcei volume is very pronounced and the expansion measured from 898 ± 154 µm 3 in the controls to 5324 ± 894 µm 3 of the drug treated A549 cells; a 6-fold increase.…”

Section: Resultsmentioning

confidence: 99%

Polyphosphate Reverses the Toxicity of the Quasi-Enzyme Bleomycin on Alveolar Endothelial Lung Cells In Vitro

Müller

Neufurth

Wang

et al. 2021

Cancers

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The anti-cancer antitumor antibiotic bleomycin(s) (BLM) induces athyminic sites in DNA after its activation, a process that results in strand splitting. Here, using A549 human lung cells or BEAS-2B cells lunc cells, we show that the cell toxicity of BLM can be suppressed by addition of inorganic polyphosphate (polyP), a physiological polymer that accumulates and is released from platelets. BLM at a concentration of 20 µg ml−1 causes a decrease in cell viability (by ~70%), accompanied by an increased DNA damage and chromatin expansion (by amazingly 6-fold). Importantly, the BLM-caused effects on cell growth and DNA integrity are substantially suppressed by polyP. In parallel, the enlargement of the nuclei/chromatin in BLM-treated cells (diameter, 20–25 µm) is normalized to ~12 µm after co-incubation of the cells with BLM and polyP. A sequential application of the drugs (BLM for 3 days, followed by an exposure to polyP) does not cause this normalization. During co-incubation of BLM with polyP the gene for the BLM hydrolase is upregulated. It is concluded that by upregulating this enzyme polyP prevents the toxic side effects of BLM. These data might also contribute to an application of BLM in COVID-19 patients, since polyP inhibits binding of SARS-CoV-2 to cellular ACE2.

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“…6,21 MAPK pathway activation is an important progenitor in anti-proliferation and advancement of apoptotic mechanism in cancer cells. 16 Oxidative stress helps to break the antioxidant defense of cancer cells and promote the apoptosis-inducing mechanism within the cell. 21 Increased expressions of phosphorylated JNK, ERK 1/2, and p-38 proteins with increasing concentration of matricin in the western blot analysis proved that matricin triggered apoptosis in H1299 cells through activation of MAPK pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Colorimetric assay to determine caspase-3, caspase-8, and caspase-9 levels were performed with commercial kit for apoptosis detection (Roche Diagnostics, CA, USA) following the manufacturer's protocols. The H1299 cells were pre-treated with matricin (0-80 µM) for 24 h, harvested, and thoroughly rinsed with cold PBS, subjected to colorimetric assay and measured using a UV-vis spectrophotometer following the method of Zhang et al 16 The experiments were performed in at least three replicates.…”

Section: Colorimetric Assay To Determine Apoptosis Enzyme Levelsmentioning

confidence: 99%

Anti-proliferative and apoptosis-inducing effects of matricin on human non-small cell lung cancer H1299 cells via MAPK pathway activation

Bai

Wang

et al. 2020

Eur J Inflamm

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Lung cancer in humans is majorly represented by non-small cell lung cancer cells, and there is a constant search for an efficient therapeutic approach. This study aims to find the anti-proliferative and apoptotic effects of matricin on H1299 cells via activation of MAPK pathway. Non-small cell H1299 cells were subjected to viability analysis with MTT assay and anti-proliferation analysis with different concentrations of matricin. Apoptosis was determined with annexin V/propidium iodide (PI) and flow cytometric analysis. Analysis of oxidative stress markers, reduced glutathione, lipid peroxidation (LPO), superoxide dismutase (SOD), and catalase (CAT) activities were done using standard assay kits. Apoptosis enzymes caspase-3, caspase-8, and caspase-9 levels were measured using colorimetric kit analysis. Western blot analysis on apoptotic proteins was performed to determine the involvement of MAPK pathway activation in apoptosis. Matricin significantly ( P < 0.01) exerted anti-proliferative activities on H1299 cells in a dose-dependent manner. Flow cytometric apoptosis analysis showed increasing concentrations of matricin had increased apoptosis ( P < 0.01) in the H1299 cells. Levels of oxidative stress markers were altered significantly ( P < 0.01) by matricin. Caspase-3, caspase-8, and caspase-9 levels were significantly increased ( P < 0.01) in matricin-treated H1299 cells. Western blot analysis showed decreased expression of anti-apoptotic Bcl-2, increased expressions of Bax and phosphorylated JNK, ERK 1/2, and p-38 MAPK proteins in matricin-treated H1299 cells. Matricin has significant anti-proliferative and apoptosis-inducing effects via activation of MAPK pathway in non-small cell lung cancer cells.

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Tetrazolium Violet Induced Apoptosis and Cell Cycle Arrest in Human Lung Cancer A549 Cells

Cited by 5 publications

References 31 publications

Cytotoxic Effect of Clerosterol Isolated from Codium fragile on A2058 Human Melanoma Cells

Cytotoxic Effect of Clerosterol Isolated from Codium fragile on A2058 Human Melanoma Cells

Polyphosphate Reverses the Toxicity of the Quasi-Enzyme Bleomycin on Alveolar Endothelial Lung Cells In Vitro

Anti-proliferative and apoptosis-inducing effects of matricin on human non-small cell lung cancer H1299 cells via MAPK pathway activation

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