The prognostic values of the peroxiredoxins family in ovarian cancer

Li, Saisai; Hu, Xiaoli; Zhu, Xueqiong

doi:10.1042/bsr20180667

Cited by 21 publications

(14 citation statements)

References 70 publications

(75 reference statements)

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“…In addition to its antioxidant role, overexpression of PRDXs in cancer tissue appears strongly correlated with more aggressive cancer behavior, tumor metastasis and tumornode-metastasis (TNM), indicating a possible role in the progression of tumorigenesis. [31][32][33][34] The cancer-promoting effects of the PRDXs are probably associated with the regulation of several reductant-oxidant-sensitive cellular processes, such as cell proliferation, apoptosis, and cell signaling. [31][32][33][34] In our study, TRIAP1 mediated the radiation-induced upregulation of PRDX3, PRDX4, and PRDX6 in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

“…[31][32][33][34] The cancer-promoting effects of the PRDXs are probably associated with the regulation of several reductant-oxidant-sensitive cellular processes, such as cell proliferation, apoptosis, and cell signaling. [31][32][33][34] In our study, TRIAP1 mediated the radiation-induced upregulation of PRDX3, PRDX4, and PRDX6 in NSCLC. They might enhance the cellular antioxidant capacity and promote the survival of NSCLC following irradiation.…”

Section: Discussionmentioning

confidence: 99%

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TRIAP1 knockdown sensitizes non‐small cell lung cancer to ionizing radiation by disrupting redox homeostasis

et al. 2020

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Background Radioresistance of some non‐small cell lung cancer (NSCLC) types increases the risk of recurrence or metastasis in afflicted patients, following radiotherapy. As such, further improvements to NSCLC radiotherapy are needed. The expression of oncogene TP53‐regulated inhibitor of apoptosis 1 (TRIAP1) in NSCLC is increased following irradiation. Furthermore, gene set enrichment analysis (GSEA) has suggested that TRIAP1 might be involved in maintaining redox homeostasis. This in turn might enhance cell radioresistance. Methods In this study we irradiated human NSCLC cell lines (A549 and H460), while knocking down TRIAP1, to determine whether a disrupted redox homeostasis could attenuate radioresistance. Results Irradiation notably increased both mRNA and protein levels of TRIAP1. In addition, TRIAP1 knockdown decreased the expression of several antioxidant proteins, including thioredoxin‐related transmembrane protein (TMX) 1, TMX2, thioredoxin (TXN), glutaredoxin (GLRX) 2, GLRX3, peroxiredoxin (PRDX) 3, PRDX4, and PRDX6 in A549 and H460 cells. In addition, silencing TRIAP1 impaired the radiation‐induced increase of the aforementioned proteins. Continuing along this line, we observed a radiation‐induced reduction of cell viability and invasion, as well as increased apoptosis and intracellular reactive oxygen species following TRIAP1 knockdown. Conclusions In summary, we identified TRIAP1 as a key contributor to the radioresistance of NSCLC by maintaining redox homeostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

TRIAP1 knockdown sensitizes non‐small cell lung cancer to ionizing radiation by disrupting redox homeostasis

et al. 2020

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“…Very little is known about the biological meaning of peroxiredoxins, especially that of PRDX-1, as a prognostic factor in ovarian cancer. Li et al studied the prognostic values of the peroxiredoxins family in ovarian cancer [31]. The study investigated protein expression profiles in normal ovarian tissues and cancerous ovarian tissues using the Human Protein Atlas database, and made a compilation of several available databases (Gene Expression Omnibus, the Cancer Biomedical Informatics Grid, and The Cancer Genome Atlas) to compare PRDX's expression at the mRNA level.…”

Section: Discussionmentioning

confidence: 99%

Peroxiredoxin-1 as a prognostic factor in patients with ovarian cancer

Sieńko

Przytuła

Czajkowski

et al. 2019

Ann Agric Environ Med.

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Introduction and objective. Peroxiredoxin-1 (PRDX-1) belongs to a family of antioxidant enzymes and has proved to be a versatile molecule regulating cell growth, differentiation and apoptosis. PRDX1-regulated signaling pathways play an important role in the progression and metastasis of human tumours, especially in breast, esophageal and lung cancers. The aim of the study was to evaluate the expression of PRDX-1 in ovarian cancer tissues, and to test the clinical value of PRDX-1 as a prognostic factor in this malignancy. Materials and method. PRDX-1 expression was assessed by automated immunohistochemistry in tumours taken from 55 patients with ovarian cancer during primary surgery. Specimen were formalin-fixed and preserved in paraffin-embedded blocks. The results were correlated with clinicopathological data. Results. A high expression of PRDX-1 was observed in 20% of cases, and was associated with worse compliance to chemotherapy protocol (P<0.002), worse response to chemotherapy (P<0.04), and higher levels of CA 125 after the 1 st line treatment (P<0.004). PRDX-1 positive subjects had a significantly lower 5-year disease-free survival (9.1% vs. 42.6%, P<0.01) and a lower 5-year overall survival (9.1% vs. 56.7%; P<0.002). Multivariate analysis showed that a high expression of PRDX-1 is an independent prognostic factor of poor, overall survival (P<0.002) and a disease-free survival (P<0.01). Conclusion. Results of the study show that PRDX-1 expression in tumour tissues can be another biomarker of prognosis in patients with ovarian cancer.

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“….0054 tissue(biomaker) [37] Q06830 Peroxiredoxin-1 (PRDX1) ↓ -0.03 0.16 -< 0.00010 tissue(biomaker) [38] ovarian cancer [39] Q96IU4 Protein ABHD14B…”

Section: Urine Proteome Changes In W256 Modelmentioning

confidence: 99%

Early changes in the urine proteome in a rat liver tumor model

Zhang

Gao

2019

Preprint

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Urine, as a potential biomarker source among the body fluids, can accumulate many changes in the body due to the lack of a mechanism to maintain a homeostatic state. Previous studies have demonstrated that proteomic technology can find many potential biomarkers to reflect different diseases in the urine.This study aims to detect early changes in the urinary proteome in a rat liver tumor model. The tumor model was established with the Walker-256 carcinosarcoma cell line (W256). Compared to before the injection, ninety-five differential proteins were significantly changed in the experimental rats. At day 3, twelve proteins were identified in the absence of pathological changes, and four of them were altered at all four time-points (B2MG, VCAM1, HA11, and LG3BP). Seven had previously been associated with liver cancer. At day 5, fifty-two differential proteins were identified. At day 7 and day 11, there was a significant decrease in the body weight of the rats, and tumor tissue was observed in the liver. Fifty-two and forty differential proteins were changed significantly at day 7 and day 11, respectively. Of the proteins that were identified at these three time-points, and twenty-four were reported to be associated with liver cancer. Comparing the differential urinary proteins and biological processes of liver tumor model with those in different models of W256 grown in other organs, specific differential protein patterns were found among the four models, which indicates that the differential urinary proteins can reflect the differences when the same tumor cell grown in different organs.Significance: This study demonstrated that (1) the rat liver tumor model caused early changes in urinary proteins may give new insight into the early diagnosis of liver cancer; (2) the same tumor cell grown in different organs can be reflected in differential urinary proteins.All rats were housed under a standard 12-h light/12-h dark cycle, and the room temperature and humidity were maintained at a standard level (22 ± 1 °C, 65-70%). Tumor cell line and CultureWalker 256 tumor cells were cultured in the ascitic fluid of Wistar rats. All cells were harvested from the rats who were given an intraperitoneal injection of 107 Walker 256 carcinoma cells after two cycles of 7 d cell passage. Then, W256 cells were resuspended in phosphate-buffered saline (PBS) before injection. The viability of the cells was detected by the Trypan blue exclusion test using a Neubauer chamber. Rat models of liver cancerA tumor-bearing animal model was established in this study. All Wistar rats were randomly divided into different groups: the control group (n =5), and the Walker-256 (W256) tumor-bearing group (n =12).After anesthesia, the left medial lobe of the liver was exposed. W256 cells (2.5× 10 5 ) were visually injected under the hepatic capsule into this lobe. The injection volume is 0.1 ml. An equal volume of PBS was also injected into the same location of the control rats. Histological analysisIn the W256 model, the livers of the experimental and cont...

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The prognostic values of the peroxiredoxins family in ovarian cancer

Cited by 21 publications

References 70 publications

TRIAP1 knockdown sensitizes non‐small cell lung cancer to ionizing radiation by disrupting redox homeostasis

TRIAP1 knockdown sensitizes non‐small cell lung cancer to ionizing radiation by disrupting redox homeostasis

Peroxiredoxin-1 as a prognostic factor in patients with ovarian cancer

Early changes in the urine proteome in a rat liver tumor model

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