Effects of Exogenous Zinc on the Cellular Zinc Distribution and Cell Cycle of A549 Cells

Yuan, Na; Wang, Yanhong; Li, Ke-jin; Zhao, Yue; Hu, Xin; Li, Mao; Zhao, Wenjie; Lian, Hong-zhen; Zheng, Wei-juan

doi:10.1271/bbb.120216

Cited by 16 publications

(12 citation statements)

References 31 publications

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“… 13 Furthermore, the role of zinc in the development and progression of prostate cancer and its widespread antitumor efficacy have been shown in several malignancies. 14 – 17 Intracellular zinc status is associated with prostate carcinogenesis. For example, zinc deficiency contributes to tumor progression and development in cultured HRPC cells, 18 whereas increased levels of intracellular zinc decrease cancer cell proliferation and induce apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Zinc supplementation induces apoptosis and enhances antitumor efficacy of docetaxel in non-small-cell lung cancer

Koçdor¹,

Ateş²,

Aydın³

et al. 2015

DDDT

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BackgroundExposure to exogenous zinc results in increased apoptosis, growth inhibition, and altered oxidative stress in cancer cells. Previous studies also suggested that zinc sensitizes some cancer cells to cytotoxic agents depending on the p53 status. Therefore, zinc supplementation may show anticancer efficacy solely and may increase docetaxel-induced cytotoxicity in non-small-cell lung cancer cells.MethodsHere, we report the effects of several concentrations of zinc combined with docetaxel on p53-wild-type (A549) and p53-null (H1299) cells. We evaluated cellular viability, apoptosis, and cell cycle progression as well as oxidative stress parameters, including superoxide dismutase, glutathione peroxidase, and malondialdehyde levels.ResultsZinc reduced the viability of A549 cells and increased the apoptotic response in both cell lines in a dose-dependent manner. Zinc also amplified the docetaxel effects and reduced its inhibitory concentration 50 (IC50) values. The superoxide dismutase levels increased in all treatment groups; however, glutathione peroxidase was slightly increased in the combination treatments. Zinc also caused malondialdehyde elevations at 50 μM and 100 μM.ConclusionZinc has anticancer efficacy against non-small-cell lung cancer cells in the presence of functionally active p53 and enhances docetaxel efficacy in both p53-wild-type and p53-deficient cancer cells.

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Section: Introductionmentioning

confidence: 99%

Zinc supplementation induces apoptosis and enhances antitumor efficacy of docetaxel in non-small-cell lung cancer

Koçdor¹,

Ateş²,

Aydın³

et al. 2015

DDDT

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“…The concentration-dependence and tissue-specificity of the response of cells to zinc stress has been extensively studied, by our own group and others, but the kinetic effects of zinc treatment on cells has received little attention [ 32 ], [ 33 ]. Moreover, most studies designed to investigate zinc homeostasis and toxicity have focused on the differential expression of a specific protein or proteome under a fixed stimulus period, such 24 or 48 h, which are the time-points that have been frequently used for 2DE analysis [ 28 – 31 ].…”

Section: Introductionmentioning

confidence: 99%

The Kinetic Response of the Proteome in A549 Cells Exposed to ZnSO4 Stress

et al. 2015

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Zinc, an essential trace element, is involved in many important physiological processes. Cell responses to zinc stress show time-dependent effects besides concentration-dependence and tissue-specificity. Herein, we investigated the time-dependent differential expression of the proteome in A549 cells after administered with ZnSO4 for both 9 and 24 h using 2DE. 123 differentially expressed protein spots were detected, most of which were up-regulated by Zn2+ treatment. Interestingly, 49 proteins exhibited significant differential expression repeatedly during these two treatment periods, and moreover showed a conserved change with different ratios and four time-dependent expression patterns. Pattern 1 (up-regulated with rapid initial induction and subsequent repression) and pattern 4 (down-regulated with steady repression) were the predominant expression patterns. The abundances of the proteins in patterns 1 and 4 after 24 h of zinc treatment are always lower than that after 9 h, indicating that exogenous zinc reduced the expression of proteins in cells after 24 h or longer. Importantly, these findings could also reflect the central challenge in detecting zinc homeostasis proteins by 2DE or other high throughput analytical methods resulting from slight variation in protein expression after certain durations of exogenous zinc treatment and/or low inherent protein content in cells. These time-dependent proteome expression patterns were further validated by measuring dynamic changes in protein content in cells and in expression of two proteins using the Bradford method and western blotting, respectively. The time-dependent changes in total zinc and free Zn2+ ion contents in cells were measured using ICP-MS and confocal microscopy, respectively. The kinetic process of zinc homeostasis regulated by muffling was further revealed. In addition, we identified 50 differentially expressed proteins which are predominantly involved in metabolic process, cellular process or developmental process, and function as binding, catalytic activity or structural molecule activity. This study further elucidates our understanding of dynamic nature of the cellular response to zinc stress and the mechanism of zinc homeostasis.

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“…The selected concentration of zinc sulfate was based on the mean of our IC50 values [12]. However, Yuan et al [16] observed no alteration in the cell cycle of human lung adenocarcinoma (A549 cells) after treatment with lower concentrations of zinc sulfate (up to 100 µM) for 6, 12 and 24 h. Mentioned studies that are not in correlation with our results used for zinc cytotoxicity assessment rapidly grew cancerous cell lines. However, some studies [17,18] that used macrophages as an in vitro model are in accordance with our findings.…”

Section: Resultsmentioning

confidence: 52%

“…However, higher therapeutic doses (150-660 mg daily) are indicated in some diseases, for example diabetes [10], urinary aminoaciduria [5], chronic kidney disease [11] or Wilson's disease [7]. Although many in vitro studies have indicated zinc toxicity [12][13][14][15][16][17][18][19], only a few studies have focused on its nephrotoxicity [5,20]. Oral treatment with zinc can change energy metabolism and cause mitochondria and cell membrane impairment in rat kidneys via inducing nephrotoxicity [21].…”

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confidence: 99%

Impact of Zinc Sulfate Exposition on Viability, Proliferation and Cell Cycle Distribution of Epithelial Kidney Cells

Marcinčáková

Schusterová

Mudroňová

et al. 2019

Pol. J. Environ. Stud.

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Effects of Exogenous Zinc on the Cellular Zinc Distribution and Cell Cycle of A549 Cells

Cited by 16 publications

References 31 publications

Zinc supplementation induces apoptosis and enhances antitumor efficacy of docetaxel in non-small-cell lung cancer

Zinc supplementation induces apoptosis and enhances antitumor efficacy of docetaxel in non-small-cell lung cancer

The Kinetic Response of the Proteome in A549 Cells Exposed to ZnSO4 Stress

Impact of Zinc Sulfate Exposition on Viability, Proliferation and Cell Cycle Distribution of Epithelial Kidney Cells

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Effects of Exogenous Zinc on the Cellular Zinc Distribution and Cell Cycle of A549 Cells

Cited by 16 publications

References 31 publications

Zinc supplementation induces apoptosis and&nbsp;enhances antitumor efficacy of docetaxel in&nbsp;non-small-cell lung cancer

Zinc supplementation induces apoptosis and&nbsp;enhances antitumor efficacy of docetaxel in&nbsp;non-small-cell lung cancer

The Kinetic Response of the Proteome in A549 Cells Exposed to ZnSO4 Stress

Impact of Zinc Sulfate Exposition on Viability, Proliferation and Cell Cycle Distribution of Epithelial Kidney Cells

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Zinc supplementation induces apoptosis and enhances antitumor efficacy of docetaxel in non-small-cell lung cancer

Zinc supplementation induces apoptosis and enhances antitumor efficacy of docetaxel in non-small-cell lung cancer