Expression of Stress-related Genes in a Cadmium-resistant A549 Human Cell Line

Croute, F.; Beau, Bernadette; Murat, J.C.; Vincent, Christian; Komatsu, Hiroyoshi; Obata, Fumiya; Soleilhavoup, J.P.

doi:10.1080/15287390590925447

Cited by 38 publications

(19 citation statements)

References 48 publications

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“…Synthesis of Hsp27 and ␣B-crystallin, 2 other sHSPs, has been reported to be induced in different cell types by various metal toxicants, including Cd, arsenite, and mercury (Pittenger et al 1992;Head et al 1996;Bonham et al 2003;Croute et al 2005;Eichler et al 2005). That Cd treatment did not result in any detectable induction of Hsp27 in the experiments of this study also could be related to the nature of the MCF-7 cell line used, as mentioned above.…”

Section: Discussionmentioning

confidence: 42%

Induction of Hsp22 (HspB8) by estrogen and the metalloestrogen cadmium in estrogen receptor– positive breast cancer cells

et al. 2007

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Estrogen (E 2 ) plays a critical role in the etiology and progression of human breast cancer. The estrogenic response is complex and not completely understood, including in terms of the involved responsive genes. Here we show that Hsp22 (synonyms: HspB8, E2IG1, H11), a member of the small heat shock protein (sHSP) superfamily, was induced by E 2 in estrogen receptor-positive MCF-7 breast cancer cells, resulting in an elevated Hsp22 protein level, whereas it was not induced in estrogen receptor-negative MDA-MB-231 cells. This induction was prevented by the pure anti-estrogen ICI182780 (faslodex, fulvestrant), whereas tamoxifen, a substance with mixed estrogenic and antiestrogenic properties, had no major inhibitory effect on this induction, nor did it induce Hsp22 on its own. Cadmium (Cd) is an environmental pollutant with estrogenic properties (metalloestrogen) that has been implicated in breast cancer. Treatment of MCF-7 cells with Cd also resulted in induction of Hsp22, and this induction was also inhibited by ICI182780. In live MCF-7 cells, Hsp22 interacted at the level of dimers with Hsp27, a related sHSP, as was shown by quantitative fluorescence resonance energy transfer measurements. In cytosolic extracts of MCF-7 cells, most of the E 2 -and Cd-induced Hsp22 was incorporated into high-molecular mass complexes. In part, Hsp22 and Hsp27 were components of distinct populations of these complexes. Finally, candidate elements in the Hsp22 promoter were identified by sequence analysis that could account for the induction of Hsp22 by E 2 and Cd. Taken together, Hsp22 induction represents a new aspect of the estrogenic response with potential significance for the biology of estrogen receptorpositive breast cancer cells.

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Section: Discussionmentioning

confidence: 42%

Induction of Hsp22 (HspB8) by estrogen and the metalloestrogen cadmium in estrogen receptor– positive breast cancer cells

et al. 2007

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“…Cd administration generates ROS in the cellular level (Yang et al 1997;Wang et al 2004), and associated to decrease of reduced glutathione and increase of lipid peroxidation (Abe et al 1994;Shaikh et al 1999;Bagchi et al 1996;Gaubin et al 2000;Croute et al 2005). Furthermore, it has been reported that hemorrhagic necrosis and apoptosis in the testis caused by Cd treatment decreased antioxidizing enzymes (Omaye 1975;Sato et al 1983;Klimczak et al 1984;Sugawara and Sugawara 1984;Sarkar et al 1998;Oteiza et al 1999).…”

Section: Discussionmentioning

confidence: 90%

“…Furthermore, Cd administration consequently to increase the resistance to the metal by scavenging reactive oxygen species (ROS), and iron (Fe), copper (Cu), and zinc (Zn) levels in testicular tissues were significantly changed by Cd exposure (Ochi et al 1983;Maitani and Suzuki 1986;Wahba and Waalkes 1990;Manca et al 1991;Hatcher et al 1995;Mikhailova et al 1997;Shaikh et al 1999;Yiin et al 1999;Gaubin et al 2000;Croute et al 2005).…”

Section: Introductionmentioning

confidence: 98%

The changes of heavy metal and metallothionein distribution in testis induced by cadmium exposure

et al. 2007

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Cadmium (Cd) is known to cause various disorders in the testis, and metallothionein (MT) is known as a protein, which has a detoxification function for heavy metals. However, the changes of Fe, Cu, and Zn distribution in the testis induced by Cd exposure have not been well examined. Moreover, only a few studies have been reported on the localization of MT after Cd exposure. In this study, we have investigated the changes of Fe, Cu, and Zn distribution in Cd-exposed testis by a newly developed in air micro-Particle Induced X-ray Emission (PIXE) method. Also, we examined the distribution of MT expression in testis. In the testis of Cd-treated rats with significant increases of lipid peroxidation, the sertoli cell tight junction was damaged by Cd exposure, resulting from disintegration of the blood testis barrier (BTB). Evaluation by in air micro-PIXE method revealed that Cd and Fe distribution were increased in the interstitial tissues and seminiferous tubules. The histological findings indicated that the testicular tissue damage was advanced, which may have been caused by Fe flowing into seminiferous tubules followed by disintegration of the BTB. As a result, Fe was considered to enhance the tissue damage caused by Cd exposure. MT was detected in spermatogonia, spermatocytes, and Sertoli's cells in the testis of Cd-treated rats, but was not detected in interstitial tissues. These results suggested that MT was induced by Cd in spermatogonia, spermatocytes, and Sertoli's cells, and was involved in the resistance to tissue damage induced by Cd.

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“…In microarray analyses, the expression of heme oxygenase-1, oxidative stress protein A170, heat-shock proteins, and oxidative DNA damage responsive GADD45, GADD153, are increased following Cd overload; while the expression of genes encoding metabolism are generally suppressed in an attempt to switch the cellular energy to overcome oxidative stress (Liu et al, 2002; Regunathan et al, 2003; Zhou et al, 2004; Croute et al, 2005). In the cultured cells, Cd increases the expression of genes related to cellular redox status, such as heme oxygenase-1, GSH S-transferases, metallothionein (MT), NAD(P)H:quinone oxidoreductase, and other stress genes (Hart et al, 1999; Yang et al, 2007, He et al, 2008).…”

Section: Oxidative Stress and Acute CD Overloadmentioning

confidence: 99%

Role of oxidative stress in cadmium toxicity and carcinogenesis

Liu

Kadiiska

2009

Toxicology and Applied Pharmacology

751

373

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Cadmium (Cd) is a toxic metal, targeting the lung, liver, kidney, and testes following acute intoxication, and causing nephrotoxicity, immunotoxicity, osteotoxicity and tumors after prolonged exposures. Reactive oxygen species (ROS) are often implicated in Cd toxicology. This minireview focused on direct evidence for the generation of free radicals in intact animals following acute Cd overload and discussed the association of ROS in chronic Cd toxicity and carcinogenesis. Cd-generated superoxide anion, hydrogen peroxide, and hydroxyl radicals in vivo have been detected by the electron spin resonance spectra, which are often accompanied by activation of redox sensitive transcription factors (e.g., NF-κB, AP-1 and Nrf2) and alteration of ROS-related gene expression. It is generally agreed upon that oxidative stress plays important roles in acute Cd poisoning. However, following long-term Cd exposure at environmentally-relevant low levels, direct evidence for oxidative stress is often obscure. Alterations in ROS-related gene expression during chronic exposures are also less significant compared to acute Cd poisoning. This is probably due to induced adaption mechanisms (e.g, metallothionein and glutathione) following chronic Cd exposures, which in turn diminish Cd-induced oxidative stress. In chronic Cd-transformed cells, less ROS signals are detected with fluorescence probes. Acquired apoptotic tolerance renders damaged cells to proliferate with inherent oxidative DNA lesions, potentially leading to tumorigenesis. Thus, ROS are generated following acute Cd overload and plays important roles in tissue damage. Adaptation to chronic Cd exposure reduces ROS production, but acquired Cd tolerance with aberrant gene expression plays important roles in chronic Cd toxicity and carcinogenesis.

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Expression of Stress-related Genes in a Cadmium-resistant A549 Human Cell Line

Cited by 38 publications

References 48 publications

Induction of Hsp22 (HspB8) by estrogen and the metalloestrogen cadmium in estrogen receptor– positive breast cancer cells

Induction of Hsp22 (HspB8) by estrogen and the metalloestrogen cadmium in estrogen receptor– positive breast cancer cells

The changes of heavy metal and metallothionein distribution in testis induced by cadmium exposure

Role of oxidative stress in cadmium toxicity and carcinogenesis

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