Peroxiredoxin I expression in human thyroid tumors

Yanagawa, Toru; Ishikawa, Tomoyoshi; Ishii, Tetsuro; Tabuchi, Katsuhiko; Iwasa, Satoshi; Bannai, Shiro; Omura, Ken; Suzuki, Haruhiko; Yoshida, Hiroshi

doi:10.1016/s0304-3835(99)00243-8

Cited by 104 publications

(61 citation statements)

References 18 publications

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“…At the protein level, consistent with mRNA expression, MG132 , Immenschuh et al 2002, Wijayanti et al 2008, indicating the expression of PRDX1 is inducible by various stimuli. PRDX1 expression is also elevated in most cancers, although the physiological mechanism is still unclear (Yanagawa et al 1999, Chang et al 2001, Kim et al 2003, Alfonso et al 2004, Lehtonen et al 2004, Xin et al 2005. Previous studies have reported that an increased level of PRDX1 might be involved in the protection of cancer cells against various therapeutic challenges ( Butzke et al 2004, Song et al 2009).…”

Section: Discussionmentioning

confidence: 99%

“…Analysis of cells and mice lacking PRDX1 suggest that it not only regulates H 2 O 2 levels, but also possesses the properties of a tumor suppressor (Neumann et al 2003), which was further supported by the finding that PRDX1 interacts with c-Myc, thereby selectively inhibiting c-Myc transcriptional activity (Egler et al 2005). However, many studies indicated that aberrant increased expression of PRDX1 is found in various kinds of cancers including thyroid, lung, and breast (Yanagawa et al 1999, Chang et al 2001, Kim et al 2003, Alfonso et al 2004, Lehtonen et al 2004, Xin et al 2005, which obscures its actual role in tumorigenesis. As the hypoxic and unstable oxygenation microenvironment of a tumor is one of the key factors influencing tumor growth and progression, this increase in PRDX1 expression might be an adaptive response.…”

Section: Introductionmentioning

confidence: 92%

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Suppression of MG132-mediated cell death by peroxiredoxin 1 through influence on ASK1 activation in human thyroid cancer cells

Du¹,

Yan²,

Zhang³

et al. 2010

Endocrine-Related Cancer

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Proteasome inhibitors represent a novel class of antitumor agents with pre-clinical and clinical evidence of activity against hematologic malignancies and solid tumors. However, emerging evidence indicates that antiapoptotic factors may also accumulate as a consequence of exposure to these drugs, thus it seems plausible that the activation of survival signaling cascades might compromise their antitumoral effects. Peroxiredoxins (PRDXs) are a family of thiol-containing peroxidases identified primarily by their ability to remove cellular hydroperoxides. The function of PRDX1 in particular has been implicated in regulating cell proliferation, differentiation, and apoptosis. Another important finding is that aberrant upregulation of PRDX1 has been discovered in various cancers. Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase (MAPK) kinase kinase that is regulated under conditions of cellular stress. ASK1 phosphorylates c-Jun N-terminal kinase and p38 MAPK, and elicits an apoptotic response. ASK1 activity is regulated at multiple levels, one of which is through interaction with PRDX1. In this study, for the first time we report that upregulation of PRDX1 expression was found in thyroid cancer cells treated with proteasome inhibitors, and PRDX1 knockdown resulted in accelerated proteasome inhibitor-induced cell death. In addition, we demonstrated that ASK1 activity was implicated in the PRDX1-dependent response of thyroid cancer cells to proteasome inhibitormediated cell death.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

Suppression of MG132-mediated cell death by peroxiredoxin 1 through influence on ASK1 activation in human thyroid cancer cells

Du¹,

Yan²,

Zhang³

et al. 2010

Endocrine-Related Cancer

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“…This endogenous defense system is highly expressed in certain cancers. The overexpression of PRDX1 has been noted in follicular thyroid neoplasms, thyroiditis, lung cancer, malignant mesothelioma and breast cancer (13)(14)(15)(16). Furthermore, PRDX2, 3, 5 and 6 levels were shown to be increased in malignant mesothelioma, while PRDX2 and 3 were overexpressed in breast cancer specimens compared with normal tissues (14,16).…”

Section: Introductionmentioning

confidence: 97%

Expression of cyclooxygenase-2, peroxiredoxin I, peroxiredoxin 6 and nuclear factor-κB in oral squamous cell carcinoma

2015

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Abstract. Tumor development and progression are multistep processes that involve local tumor growth and invasion, followed by metastasis. The aggressiveness of the tumor is the major determinant of the mortality of oral cancer patients. The present study investigates whether the expression levels of cyclooxygenase-2 (COX-2), nuclear factor-κB (NF-κB), peroxiredoxin 1 (PRDX1) and PRDX6 are associated with the development, proliferation, differentiation and recurrence of oral squamous cell carcinoma (OSCC). The mRNA expression levels of COX-2, NF-κB, PRDX1 and PRDX6 were examined in 50 OSCC specimens and 19 normal oral mucosae by quantitative polymerase chain reaction (qPCR). qPCR analysis showed that the mRNA levels of COX-2 in OSCC were significantly higher than those in the normal oral mucosae (P=0.021). The expression levels of PRDX1 in high-stage tumors (T3 and T4) were significantly elevated compared with those in low-stage tumors (T1) (P=0.047). Additionally, the expression levels of NF-κB in the high-grade tumor were significantly elevated compared with those in the low-grade tumors (P=0.030). Overall, it was indicated that the expression of COX-2 is strongly associated with the development of OSCC. Moreover, the enhanced expression of PRDX1 and NF-κB may function in the progression of OSCC, which serves as a useful marker for prognosis in patients with oral cancer.

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“…From these reports and our former study, Prdx1 appears to have a possible correlation with an anti-tumor effect by producing epigenetic changes in cancer patients. On the other hand, some researchers have mentioned that this protein may be involved with cell proliferation and tumor growth in several kinds of solid cancers (11)(12)(13)(14)(15).In order to contribute to the controversial discussion about the influence of Prdx1 expression in malignant tumors, we examined the expression of this protein in 114 cases of ESCC by immunohistochemistry and evaluated the correlations with the clinical parameters of ESCC to determine whether or not the expression of PrdxI in ESCC plays an important role in tumor progression. ONCOLOGY REPORTS 18: 867-871, 2007 867 Tumor suppressor Prdx1 is a prognostic factor in esophageal squamous cell carcinoma patients ISAMU HOSHINO, HISAHIRO MATSUBARA, YASUNORI AKUTSU, TAKANORI NISHIMORI, YASUO YONEYAMA, KENTARO MURAKAMI, HARUHITO SAKATA, KAZUYUKI MATSUSHITA and TAKENORI OCHIAI…”

mentioning

confidence: 99%

Tumor suppressor Prdx1 is a prognostic factor in esophageal squamous cell carcinoma patients

Hoshino¹,

Matsubara²,

Akutsu³

et al. 2007

Oncol Rep

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Abstract. Peroxiredoxins (Prdxs) are a family of antioxidant enzymes that are also known as scavengers of peroxide in mammalian cells. Some reports have shown that the overexpression of Prdx1, which is one of the peroxiredoxins that is a ubiquitously expressed protein, was related to a poor prognosis in several types of human cancers. In this study, we investigated the expression levels of Prdx1 in esophageal squamous cell carcinoma by immunohistochemistry, and the correlation between the Prdx1 expression and the clinical status was elucidated. Immunohistochemical staining was performed in 114 samples which were collected from surgical esophageal cancer specimens. Cytoplasmic staining of Prdx1 was evaluated based on the following scoring criteria: Grade I, negative or weak staining; Grade II, moderate staining; and Grade III, strong staining. The percentage of patients with a Grade I expression of Prx1 was 20% (23 of 114), 44% had Grade II (50 of 114), and 36% had Grade III (41 of 114). The Prdx1 immunoreactivity showed an inverse significant correlation with T-category (P<0.0001), lymph node metastasis (P=0.048), and stage (P=0.001). In addition, the patients with tumors exhibiting a reduced Prdx1 expression had shorter overall survival (P=0.022) in comparison to the patients with tumors which had a higher Prdx1 expression. Currently, Prdx1 has been shown to act as a tumor suppressor. Our results provide strong evidence that the reduced Prdx1 expression is an important factor in esophageal squamous cancer progression and could serve as a useful prognostic marker. IntroductionEsophageal cancer is the eighth most frequent cancer and the sixth most frequent cause of death from malignant disease in the world (1). Esophageal squamous cell carcinoma (ESCC) is the most common type in Japan (2). A large number of reports about genetic changes in ESCC have already been published, but little is known about the major tumor suppressor genes or major oncogenes in the process of tumor progression of this malignant disease. ESCC is still a fatal malignancy with a 5-year rate of 5% to 20% for advanced stage patients undergoing a curative resection (3). This miserable prognosis for ESCC involves not only the aggressive character of this tumor but also the limited number of useful markers available for diagnostic purposes.Therefore, better markers which indicate the malignant potential of ESCC should help in the prognosis or optimal treatment of the patients suffering from this disease. In this study, we focus on Prdx1, one of the peroxiredoxins (Prdxs) belonging to a novel antioxidant family, which has been reported to be a tumor suppressor gene. Prdx1 has been thought to have an inhibitory function for both c-Abl and c-Myc, of which active forms cause several neoplasms (4,5). Neumann et al (6) showed, using Prdx1 knockout mice, that Prdx1 expression correlated with the reactive oxygen species and the incidence of malignant disease. Moreover, our previous study using a cDNA microarray showed that one of the novel histone deacet...

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Peroxiredoxin I expression in human thyroid tumors

Cited by 104 publications

References 18 publications

Suppression of MG132-mediated cell death by peroxiredoxin 1 through influence on ASK1 activation in human thyroid cancer cells

Suppression of MG132-mediated cell death by peroxiredoxin 1 through influence on ASK1 activation in human thyroid cancer cells

Expression of cyclooxygenase-2, peroxiredoxin I, peroxiredoxin 6 and nuclear factor-κB in oral squamous cell carcinoma

Tumor suppressor Prdx1 is a prognostic factor in esophageal squamous cell carcinoma patients

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