ArticleFEBS open bio2013
Anti-apoptotic role of peroxiredoxin III in cervical cancer cells.
Article in FEBS open bio, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Up-regulation of peroxiredoxin 3 by high-risk human papillomavirus in cervical cancer cells.Archives of medical science : AMS · 2026Article
- Catalase S-Glutathionylation by NOX2 and Mitochondrial-Derived ROS Adversely Affects Mice and Human Neutrophil Survival.Inflammation · 2019Article
- Plasma level of peroxiredoxin 3 in patients with polycystic ovarian syndrome.BMC endocrine disorders · 2019Article
- Epigenetic regulation of peroxiredoxins: Implications in the pathogenesis of cancer.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- New Challenges to Study Heterogeneity in Cancer Redox Metabolism.Frontiers in cell and developmental biology · 2017Review
- The Tumorigenic Roles of the Cellular REDOX Regulatory Systems.Oxidative medicine and cellular longevity · 2016Review
- The functional role of peroxiredoxin 3 in reactive oxygen species, apoptosis, and chemoresistance of cancer cells.Journal of cancer research and clinical oncology · 2015Review
- Hitting the Bull's-Eye in Metastatic Cancers-NSAIDs Elevate ROS in Mitochondria, Inducing Malignant Cell Death.Pharmaceuticals (Basel, Switzerland) · 2015Review
- Metallothionein-I/II Knockout Mice Aggravate Mitochondrial Superoxide Production and Peroxiredoxin 3 Expression in Thyroid after Excessive Iodide Exposure.Oxidative medicine and cellular longevity · 2015Article
- Peroxiredoxin 3 is resistant to oxidation-induced apoptosis of Hep-3b cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014Article
- Peroxiredoxin V Inhibits Emodin-induced Gastric Cancer Cell ApoptosisIn vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a member of peroxiredoxin (Prx) family, PrxIII is predominantly located in mitochondria and plays an important role as a scavenger of reactive oxygen species (ROS). Since previous reports demonstrated over-expression of PrxIII in cervical cancer, we conducted the present study to investigate the significance of PrxIII in cervical cancer development and/or progression. Cervical cancer cells were cultured from tissues derived from cervical cancer patients. After successful knockdown of PrxIII expression by small interfering RNA, we evaluated ROS level, viable cell number, and apoptosis of cervical cancer cells along with the culture time. The production of ROS was increased in cervical cancer cells as compared with normal cervical epithelia. Knockdown of PrxIII expression induced up-regulation of other Prx members including PrxI, PrxII, and PrxV. ROS level was higher in down-regulated cervical cancer cells than in controls and the difference was increasing with culture time. We also observed increased apoptosis and decreased viable cell number in down-regulated cervical cancer cells. Our results suggest that PrxIII is an indispensable ROS scavenger, which protects tumor cells against oxidative damage and subsequent apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.