Up-regulation of hypoxia inducible factor-1α by cobalt chloride correlates with proliferation and apoptosis in PC-2 cells

Dai, Zhijun; Gao, Jie; Ma, Xiaolong; Yan, Kun; Liu, Xiaoxu; Kang, Huafeng; Ji, Zong-Zheng; Guan, Huaijin; Wang, Xijing

doi:10.1186/1756-9966-31-28

Cited by 88 publications

(88 citation statements)

References 25 publications

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“…In the case of a genetic over-stabilization of HiF-1, which is the case for various type of cancers [13,8], the increased ability of cancer cells to enter into a quiescent state is well described by our model. Indeed, this case can be modeled by multiplying [H 0 ] by an ǫ > 1 parameter to artificially increase the HiF-1 level.…”

Section: Discussionmentioning

confidence: 73%

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A mathematical model of HiF-1-mediated response to hypoxia on the G1/S transition

Bedessem

Stéphanou

2014

Mathematical Biosciences

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Hypoxia is known to influence the cell cycle by increasing the G1 phase duration or by inducing a quiescent state (arrest of cell proliferation). This entry into quiescence is a mean for the cell to escape from hypoxia-induced apoptosis. It is suggested that some cancer cells have gain the advantage over normal cells to easily enter into quiescence when environmental conditions, such as oxygen pressure, are unfavorable [43,1]. This ability contributes in the appearance of highly resistant and aggressive tumor phenotypes [2].The HiF-1α factor is the key actor of the intracellular hypoxia pathway.As tumor cells undergo chronic hypoxic conditions, HiF-1α is present in higher level in cancer than in normal cells. Besides, it was shown that genetic mutations promoting overstabilization of HiF-1α are a feature of various types of cancers [8]. Finally, it is suggested that the intracellular level of HiF-1α can be related to the aggressiveness of the tumors [53,24,4,10] However, up to now, mathematical models describing the G1/S transition under hypoxia, did not take into account the HiF-1α factor in the hypoxia pathway.Therefore, we propose a mathematical model of the G1/S transition under hypoxia, which explicitly integrates the HiF-1α pathway. The model reproduces the slowing down of G1 phase under moderate hypoxia, and the entry into quiescence of proliferating cells under severe hypoxia. We show how the inhibition of cyclin D by HiF-1α can induce quiescence; this result provides a theoretical explanation to the experimental observations of Wen et al. (2010). Thus, our model confirms that hypoxia-induced chemoresistance can be linked, for a part, to the negative regulation of cyclin D by HiF-1α.

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Section: Discussionmentioning

confidence: 73%

“…In other cases, genetic mutations induce an over-stabilization of HiF-1. It is the case for the renal clear carcinoma [13]. As a consequence, for the same oxygen pressure, HiF-1 will have a higher level in cancer cells than in normal cells [15].…”

mentioning

confidence: 94%

A mathematical model of HiF-1-mediated response to hypoxia on the G1/S transition

Bedessem

Stéphanou

2014

Mathematical Biosciences

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“…The effects of chemically induced hypoxia can be achieved by treating cells with deferoxamine (Guo et al, 2006) or dimethyloxalylglycine (Elvidge et al, 2006). Here, hypoxia was induced using a hypoxia chamber or CoCl 2 (Dai et al, 2012). Previous studies have reported that these methods have a similar effect on cells in creating a low-oxygen environment.…”

Section: Discussionmentioning

confidence: 99%

Ursodeoxycholic acid upregulates ERK and Akt in the protection of cardiomyocytes against CoCl2

Hanafi

Noor

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Ursodeoxycholic acid (UDCA) is used to treat liver diseases and demonstrates cardioprotective effects. Accumulation of the plasma membrane sphingolipid sphingomyelin in the heart can lead to atherosclerosis and coronary artery disease. Sphingomyelinases (SMases) break down sphingomyelin, producing ceramide, and inhibition of SMases activity can promote cell survival. We hypothesized that UDCA regulates activation of ERK and Akt survival signaling pathways and SMases in protecting cardiac cells against hypoxia. Neonatal cardiomyocytes were isolated from 0-to 2-day-old Sprague Dawley rats, and given 100 µM CoCl 2 , 150 µM H 2 O 2 , or placed in a hypoxia chamber for 24 h. The ameliorative effects of 100-µM UDCA treatment for 12 h were then assessed using MTS, QuantiGene Plex (for Smpd1 and Smpd2), and SMase assays, beating rate assessment, and western blotting (for ERK and Akt). Data were analyzed by the paired Student t-tests and one-way analyses of variance. Cell viability decreased significantly after H 2 O 2 (85%), CoCl 2 (50%), and hypoxia chamber (52%) treatments compared to the untreated control (100%). UDCA significantly counteracted the effects of chamber-and CoCl 2 -induced hypoxia on viability and beating rate. However, no significant differences were observed in acid SMase gene and protein expression between the untreated, CoCl 2 , and UDCA-CoCl 2 groups. In contrast, neutral SMase gene and protein expression did significantly differ between the latter two groups. ERK and Akt phosphorylation was higher in hypoxic cardiomyocytes treated with UDCA than those given CoCl 2 alone. In conclusion, UDCA regulates the activation of survival signaling proteins and SMases in neonatal rat cardiomyocytes during hypoxia.

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“…Der effektivste Zellverlust wurde in ei nem Kobaltchlorid (CoCl 2 )-Degene rations modell erreicht. Hier bei wird in der Zelle chemisch eine Hypoxie induziert [10]. …”

Section: Startschuss Fürunclassified

Campus

2017

Kompass Ophthalmol

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Up-regulation of hypoxia inducible factor-1α by cobalt chloride correlates with proliferation and apoptosis in PC-2 cells

Cited by 88 publications

References 25 publications

A mathematical model of HiF-1-mediated response to hypoxia on the G1/S transition

A mathematical model of HiF-1-mediated response to hypoxia on the G1/S transition

Ursodeoxycholic acid upregulates ERK and Akt in the protection of cardiomyocytes against CoCl2

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