Involvement of sulfhydryl oxidase QSOX1 in the protection of cells against oxidative stress-induced apoptosis

Morel, Carole; Adami, Pascale; Musard, Jean-François; Duval, Dominique; Radom, Jean; Jouvenot, Michèle

doi:10.1016/j.yexcr.2007.09.003

Cited by 44 publications

(50 citation statements)

References 27 publications

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“…They found that expression of QSOX1 directly correlates with an increase in cell survival after treatment with H 2 O 2 (15). These findings may suggest that increased QSOX1 expression in tumor cells allows them to actively evade cellular apoptotic mechanisms mediated by reactive oxygen species.…”

Section: Introductionmentioning

confidence: 95%

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Quiescin Sulfhydryl Oxidase 1 Promotes Invasion of Pancreatic Tumor Cells Mediated by Matrix Metalloproteinases

Katchman

Antwi

Hostetter

et al. 2011

Molecular Cancer Research

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Quiescin sulfhydryl oxidase 1 (QSOX1) oxidizes sulfhydryl groups to form disulfide bonds in proteins. We previously mapped a peptide in plasma from pancreatic ductal adenocarcinoma (PDA) patients back to an overexpressed QSOX1 parent protein. In addition to overexpression in pancreatic cancer cell lines, 29 of 37 patients diagnosed with PDA expressed QSOX1 protein in tumor cells, but QSOX1 was not detected in normal adjacent tissues or in a transformed, but nontumorigenic cell line. To begin to evaluate the advantage QSOX1 might provide to tumors, we suppressed QSOX1 protein expression using short hairpin (sh) RNA in two pancreatic cancer cell lines. Growth, cell cycle, apoptosis, invasion, and matrix metalloproteinase (MMP) activity were evaluated. QSOX1 shRNA suppressed both short and long isoforms of the protein, showing a significant effect on cell growth, cell cycle, and apoptosis. However, QSOX1 shRNA dramatically inhibited the abilities of BxPC-3 and Panc-1 pancreatic tumor cells to invade through Matrigel in a modified Boyden chamber assay. Mechanistically, gelatin zymography indicated that QSOX1 plays an important role in activation of MMP-2 and MMP-9. Taken together, our results suggest that the mechanism of QSOX1-mediated tumor cell invasion is by activation of MMP-2 and MMP-9. Mol Cancer Res; 9(12); 1621-31. Ó2011 AACR.

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Section: Introductionmentioning

confidence: 95%

“…A recent publication by Morel and colleagues highlighted the role of QSOX1 in protecting MCF7 breast tumor cells from oxidative stress-induced apoptosis (15). They found that expression of QSOX1 directly correlates with an increase in cell survival after treatment with H 2 O 2 (15).…”

Section: Introductionmentioning

confidence: 99%

Quiescin Sulfhydryl Oxidase 1 Promotes Invasion of Pancreatic Tumor Cells Mediated by Matrix Metalloproteinases

Katchman

Antwi

Hostetter

et al. 2011

Molecular Cancer Research

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“…Cell proliferation assay MCF-7-Flag-GEC1-(His) 6 (clones 1 and 2) and MCF-7-pcDNA cell lines were plated in 96-well plates (3000 cells per well) and cell proliferation experiments were conducted over a 10-day period using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) (Sigma-Aldrich) (Morel et al, 2007). For each clone, two independent experiments were performed in 16 wells.…”

Section: Experimental Analysismentioning

confidence: 99%

High expression of gabarapl1 is associated with a better outcome for patients with lymph node-positive breast cancer

et al. 2010

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BACKGROUND: This study evaluates the relation of the early oestrogen-regulated gene gabarapl1 to cellular growth and its prognostic significance in breast adenocarcinoma. METHODS: First, the relation between GABARAPL1 expression and MCF-7 growth rate was analysed. Thereafter, by performing macroarray and reverse transcriptase quantitative-polymerase chain reaction (RT -qPCR) experiments, gabarapl1 expression was quantified in several histological breast tumour types and in a retrospective cohort of 265 breast cancers. RESULTS: GABARAPL1 overexpression inhibited MCF-7 growth rate and gabarapl1 expression was downregulated in breast tumours. Gabarapl1 mRNA levels were found to be significantly lower in tumours presenting a high histological grade, with a lymph nodepositive (pN þ ) and oestrogen and/or progesterone receptor-negative status. In univariate analysis, high gabarapl1 levels were associated with a lower risk of metastasis in all patients (hazard ratio (HR) 4.96), as well as in pN þ patients (HR 14.96). In multivariate analysis, gabarapl1 expression remained significant in all patients (HR 3.63), as well as in pN þ patients (HR 5.65). In univariate or multivariate analysis, gabarapl1 expression did not disclose any difference in metastasis risk in lymph node-negative patients. CONCLUSIONS: Our data show for the first time that the level of gabarapl1 mRNA expression in breast tumours is a good indicator of the risk of recurrence, specifically in pN þ patients.

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“…It was found that the expression level of glutathione S-transferase zeta 1 in young rat hearts was up-regulated at 6 h after APC. Quiescin Q6, found to be protective against oxidative stress (Morel et al 2007;Li et al 2005), was up-regulated at 12 h after APC. Hypoxia up-regulated 1, which promotes cell survival in hypoxic condition (Tamatani et al 2001;Ozawa et al 2001;Kuwabara et al 1996), was up-regulated at 12 h after APC.…”

Section: Discussionmentioning

confidence: 96%

Age-associated differences in gene expression in response to delayed anesthetic preconditioning

Zhong

Fleming

et al. 2011

AGE

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Involvement of sulfhydryl oxidase QSOX1 in the protection of cells against oxidative stress-induced apoptosis

Cited by 44 publications

References 27 publications

Quiescin Sulfhydryl Oxidase 1 Promotes Invasion of Pancreatic Tumor Cells Mediated by Matrix Metalloproteinases

Quiescin Sulfhydryl Oxidase 1 Promotes Invasion of Pancreatic Tumor Cells Mediated by Matrix Metalloproteinases

High expression of gabarapl1 is associated with a better outcome for patients with lymph node-positive breast cancer

Age-associated differences in gene expression in response to delayed anesthetic preconditioning

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