Thioredoxin Peroxidase-1 (peroxiredoxin-1) Is Increased in Thioredoxin-1 Transfected Cells and Results in Enhanced Protection against Apoptosis Caused by Hydrogen Peroxide but Not by Other Agents Including Dexamethasone, Etoposide, and Doxorubicin

Berggren, Margareta; Husbeck, Bryan; Samulitis, Betty K.; Baker, Amanda F.; Gallegos, Alfred; Powis, Garth

doi:10.1006/abbi.2001.2435

Cited by 108 publications

(69 citation statements)

References 44 publications

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“…The same report also documented that overexpression of Prx-II protected cells from gamma irradiation. Cytoprotection by Prx-II in response to numerous stimuli has been well documented by others (Iwahara et al, 1995;Netto et al, 1996;Berggren et al, 2001) and by us . In contrast to the results of Park et al, our results showed that Prx-I, instead of Prx-II, expression was induced by ionizing radiation in human HT29 and rat C6 glioma cells.…”

Section: Discussionsupporting

confidence: 52%

Induction of radioprotective peroxiredoxin‐I by ionizing irradiation

Chen

McBride

Iwamoto

et al. 2002

J of Neuroscience Research

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Results of this study indicate a radioprotective effect of peroxiredoxin-I. Peroxiredoxin-I is an antioxidant that scavenges hydroperoxides, whereas reactive oxygen species are the main mediators of ionizing radiation toxicity. We hypothesized that peroxiredoxin-I might be induced by cellular exposure to radiation and act to protect them against its cytotoxic effects. Western blot and Northern blot analyses were used to assess peroxiredoxin-I protein and mRNA expression. Rat C6 glioma cells were engineered to overexpress sense or antisense human peroxiredoxin-I using retroviral vectors. Clonogenic cell survival was used to assess radiosensitivities of the engineered cells. Ionizing radiation induced peroxiredoxin-I protein and mRNA expression in human HT29 colon cancer and rat C6 glioma cells in a dose-and time-dependent manner over a 24 hr period. To determine the effect of peroxiredoxin-I on radiation responses, C6 glioma cells were engineered to overexpress sense or antisense human peroxiredoxin-I. In clonogenic assays, cells overexpressing peroxiredoxin-I were more radioresistant. Cells transduced with antisense peroxiredoxin-I were marginally more sensitive to radiation toxicity. Irradiation can induce peroxiredoxin-I expression, and the increased peroxiredoxin-I may protect cells from further radiation damage. These results suggest that protection by peroxiredoxin-I may play an important role in the survival of glioma and colon cancer cells in patients undergoing radiation therapy.

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Section: Discussionsupporting

confidence: 52%

Induction of radioprotective peroxiredoxin‐I by ionizing irradiation

Chen

McBride

Iwamoto

et al. 2002

J of Neuroscience Research

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“…Although Bcl-2, Bax, or Trx levels could not individually explain such variation, a composite of their actions may have influenced outcome, with Bcl-2 and Trx contributing resistance and Bax conferring sensitivity. Trx confers survival directly to chronic lymphocytic leukemia cells (29), and by up-regulating Trx peroxidase-1 it protects murine lymphoma cells from ''apoptosis caused by H 2 O 2 but not by other agents'' (30). Bcl-2 has been implicated in potentiating a cell's antioxidant capacity with its actions; in turn, it is counteracted by Bax (31).…”

Section: Discussionmentioning

confidence: 99%

Dopamine targets cycling B cells independent of receptors/transporter for oxidative attack: Implications for non-Hodgkin’s lymphoma

Meredith

Holder

Rosén

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Human B lymphocytes and derived lines from a spectrum of B cell malignancy were studied for expression of dopaminergic pathway components and for their cytostatic response to the catecholamine and related, potentially therapeutic compounds. Proliferating normal lymphocytes and dividing malignant clones rapidly arrested on exposure to dopamine in the low (<10 M) micromolar range. The antiparkinsonian drugs L-DOPA and apomorphine (particularly) were similarly antiproliferative. With the exception of D4, dopamine receptors D1-D5 were variably expressed among normal and neoplastic B cell populations, as was the dopamine transporter. Transcripts for D1 and D2 were frequently found, whereas D3 and D5 revealed restricted expression; dopamine transporter was detected in most cases. Nevertheless, pharmacological analysis disclosed that dopamine targeted cycling B cells independent of these structures. Rather, oxidative stress constituted the primary mechanism: the catecholamine's actions being mimicked by hydrogen peroxide and reversed by exogenous catalase, and evidence for the intracellular redox protein thioredoxin contributing protection. Among proliferating clones, growth arrest was accompanied by cell death in populations deplete in antiapoptotic Bcl-2: resting lymphocytes escaping low micromolar dopamine toxicity. Dysregulated bcl-2 expression, although preventing oxidative-induced caspase-dependent apoptosis, by itself conferred only minor protection against dopamine cytostasis. The selective impact of dopamine on lymphocytes that are in active cycle indicates an axis for therapeutic intervention not only in B cell neoplasia but also in lymphoproliferative disturbances generally. Rational tailoring of drug delivery systems already in development for Parkinson's disease could provide ideal vehicles for carrying the oxidative hit directly to the target populations.apoptosis ͉ oxidative stress ͉ Parkinson's disease ͉ Bcl-2 ͉ monoamines

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“…The CCNC gene has been shown to be deleted in acute lymphoblastic leukemias 34) and thiol-containing proteins with antioxidant capacity have recently been characterized and shown to be overexpressed in a number of human malignancies. 35) There is no evidence, however, that these genes participate in prostate carcinogenesis. The glutamate receptor 6 (GluR6, GRIK2) gene, which has been linked to autism, is also located on 6q21.…”

Section: Discussionmentioning

confidence: 99%

Genetic mapping of allelic loss on chromosome 6q within heterogeneous prostate carcinoma

et al. 2003

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A number of genetic events have been reported in prostate carcinogenesis, including frequent loss of heterozygosity (LOH) on chromosomes 8q, 10q, 16q and 18q. In samples of heterogeneous, multifocal prostate carcinomas, we focused on chromosome 6q using PCR-based techniques with 15 microsatellite markers to identify the specific 6q deletion within tumors. LOH of one or more polymorphic markers was detected in 10 of 21 tumors (48%). Two of these 10 tumors demonstrated LOH in all cancerous foci at specific loci and 4 tumors showed deletion in one focus. Different deletion patterns were found in 3 tumors when different polymorphic markers were used. In 90% of tumors showing LOH in one or more foci, however, two common regions of LOH were identified; one at 1.81 cM on 6q15-16.3 between markers D6S1631 and D6S1056, and the other at 5.11 cM on 6q16-21 between markers D6S424 and D6S283. By RT-PCR analysis, the TAK1 gene located at these loci did not correlate with LOH status, indicating that TAK1 is not a target gene in prostate carcinoma. The 6q deletion occurs heterogeneously and LOH was more frequent in tumors of higher pathological stages, implying that this alteration is a late event in prostate carcinogenesis. ytogenetic studies of prostate carcinomas indicate that various chromosomal deletions containing tumor suppressor genes contribute to the development and progression of tumors. Recent intensive investigations using PCR of polymorphic microsatellite markers, fluorescent in situ hybridization (FISH), and comparative genomic hybridization (CGH) have shown consistent genetic alterations on chromosomes 2q, 3q, 5q, 6q, 7q, 8q, 9q, 10q, 13q, 16q and 18q.1, 2) Although malignant tumors are now believed to develop through a multi-step process involving both oncogene activation and tumor suppressor gene (TSG) inactivation, 3) putative TSG are postulated to be the primary targets of these carcinogenesis-associated events.Allelic losses on 6q have been described in a number of cancers including melanoma and breast, ovarian, and renal cancers. [4][5][6][7][8][9] Genes associated with prostate carcinoma in the 6q region have also been reported and, while the incidences varied, 6q alterations have been found to occur in up to 48% of prostate cancers.1, 2, 10, 11) However, the role of these chromosomal aberrations remains unclear. At least two common regions of 6q deletion have been identified in prostate carcinoma. Using 13 polymorphic markers, Srikantan et al.2) reported that 6q16, 6q3-21, and the distal region 6q23-24 were deleted. Hyytinen et al.11) examined two regions, 6q16-21 and 6q22, and claimed that deletion of 6q16-22 is a frequent event in prostate cancer. They further showed that loss of 6q24 was associated with androgen-independence and tumorigenicity.12) Several candidate genes, such as the insulin-like growth factor II receptor (IGF2R) at 6q26 or cyclin C (CCNC) at 6q21, may participate in prostate carcinogenesis.1) A novel gene located on chromosome 6q23-24 and designated UROC28 was recently identified as ...

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Thioredoxin Peroxidase-1 (peroxiredoxin-1) Is Increased in Thioredoxin-1 Transfected Cells and Results in Enhanced Protection against Apoptosis Caused by Hydrogen Peroxide but Not by Other Agents Including Dexamethasone, Etoposide, and Doxorubicin

Cited by 108 publications

References 44 publications

Induction of radioprotective peroxiredoxin‐I by ionizing irradiation

Induction of radioprotective peroxiredoxin‐I by ionizing irradiation

Dopamine targets cycling B cells independent of receptors/transporter for oxidative attack: Implications for non-Hodgkin’s lymphoma

Genetic mapping of allelic loss on chromosome 6q within heterogeneous prostate carcinoma

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