Peroxiredoxin I expression in oral cancer: a potential new tumor marker

Yanagawa, Toru; Iwasa, Satoshi; Ishii, Tetsuro; Tabuchi, Katsuhiko; Yusa, Hiroshi; Onizawa, Kojiro; Omura, Ken; Harada, Hiroyuki; Suzuki, Haruhiko; Yoshida, Hiroshi

doi:10.1016/s0304-3835(00)00434-1

Cited by 101 publications

(81 citation statements)

References 32 publications

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“…The overexpression of PRDX was also reported in human breast and lung cancer (16,35). In OSCC, Yanagawa et al studied PRDX1 expression for the first time and found low PRDX1expression levels to be associated with larger tumor masses, lymph node metastases and poorly-differentiated tumors (36). This data is contrary to previous studies and the present result showing that the PRDX1 mRNA expression was elevated in larger tumors (P=0.047).…”

Section: Discussioncontrasting

confidence: 95%

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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Section: Discussioncontrasting

confidence: 95%

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

2015

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“…The present study has identified at least 10 genes whose mutations increased GCR rates and the human homologs of which might be found in GCR-prone human cancers. Indeed, there have been many recent reports (46)(47)(48)(49)(50)(51) supporting the concept that genes identified in our screen have importance in cancer development. Abnormal expression of human TSA1 in many different cancers and severe hemolytic anemia and several malignant cancers in mice lacking murine homolog of TSA1 gene, Prdx1, were observed.…”

Section: Discussionsupporting

confidence: 78%

Mutator genes for suppression of gross chromosomal rearrangements identified by a genome-wide screening in Saccharomyces cerevisiae

Smith

Hwang

Banerjee

et al. 2004

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

136

151

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Different types of gross chromosomal rearrangements (GCRs), including translocations, interstitial deletions, terminal deletions with de novo telomere additions, and chromosome fusions, are observed in many cancers. Multiple pathways, such as S-phase checkpoints, DNA replication, recombination, chromatin remodeling, and telomere maintenance that suppress GCRs have been identified. To experimentally expand our knowledge of other pathway(s) that suppress GCRs, we developed a generally applicable genome-wide screening method. In this screen, we identified 10 genes (ALO1, CDC50, CSM2, ELG1, ESC1, MMS4, RAD5, RAD18, TSA1, and UFO1) that encode proteins functioning in the suppression of GCRs. Moreover, the breakpoint junctions of GCRs from these GCR mutator mutants were determined with modified breakpoint-mapping methods. We also identified nine genes (AKR1, BFR1, HTZ1, IES6, NPL6, RPL13B, RPL27A, RPL35A, and SHU2) whose mutations generated growth defects with the pif1⌬ mutation. In addition, we found that some of these mutations changed the telomere size.

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“…Thus, Prdx1 is a potent tumor suppressor gene. It was also reported that lower expression of Prdx1 in the tumor correlates to larger tumor size, lymph node metastasis, and clinically advanced stages (24), and that Prdx1 knockout mice generate malignancies in intestines, lymphomas, and sarcomas (25).…”

Section: Discussionmentioning

confidence: 97%

Histone Deacetylase Inhibitor FK228 Activates Tumor Suppressor Prdx1 with Apoptosis Induction in Esophageal Cancer Cells

Hoshino

Matsubara

Hanari

et al. 2005

Clinical Cancer Research

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Purpose: The histone deacetylase inhibitor FK228 shows strong activity as a potent antitumor drug but its precise mechanism is still obscure. The purpose of this study is to reveal the effect of FK228 on gene expression in the cell and to determine the mechanism of the antitumor activity of FK228 for further clinical applications. Experimental Design and Results: Microarray analysis was applied to verify the gene expression profiles of 4,608 genes after FK228 treatment using human esophageal squamous cell cancer cell lines T.Tn and TE2. Among them, peroxiredoxin 1 (Prdx1), a member of the peroxiredoxin family of antioxidant enzymes having cell growth suppression activity, as well as p21 WAF1 , were significantly activated by FK288. In addition, FK228 strongly inhibited the cell growth of T.Tn and TE2 by the induction of apoptosis. Further, chromatin immunoprecipitation analysis revealed that FK228 induced the accumulation of acetylated histones H3 and H4 in Prdx1 promoter, including the Sp1-binding site. In mouse xenograft models of T.Tn and TE2 cells, FK228 injection resulted in significant tumor regression as well as activated Prdx1 expression in tumor tissues. Prdx1 suppression by RNA interference hindered the antitumor effect of FK228. Conclusion: Our results indicate that the antitumor effect of FK228 in esophageal cancer cells is shown at least in part through Prdx1 activation by modulating acetylation of histones in the promoter, resulting in tumor growth inhibition with apoptosis induction.

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Peroxiredoxin I expression in oral cancer: a potential new tumor marker

Cited by 101 publications

References 32 publications

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

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

Mutator genes for suppression of gross chromosomal rearrangements identified by a genome-wide screening in Saccharomyces cerevisiae

Histone Deacetylase Inhibitor FK228 Activates Tumor Suppressor Prdx1 with Apoptosis Induction in Esophageal Cancer Cells

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