Downregulation of Peroxiredoxin I by a Novel Fully Human Phage Display Recombinant Antibody Induces Apoptosis and Enhances Radiation Sensitization in A549 Lung Carcinoma Cells

Guo, Qishuai; Huang, Xi; Zhang, Jun; Luo, Yi; Peng, Zhiping; Li, Shaolin

doi:10.1089/cbr.2011.0989

Cited by 11 publications

(6 citation statements)

References 31 publications

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“…Thus, it is also possible for Srx inhibitor to inhibit the peroxidase function of 2-Cys Prxs by impeding deglutathionylation. 2-Cys Prxs have been implicated in cancer development and maintenance; 2-Cys Prxs were highly expressed in a variety of cancer cells and tumor tissues [39][40][41][42][43] and downregulation of PrxI in lung cancer cells promoted apoptosis and radiosensitivity [44,45]. Therefore, Srx inhibitor might cause a decline in the peroxidase activity of 2-Cys Prx, which results in oxidative stress and thereby, apoptosis of cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Sulfiredoxin inhibitor induces preferential death of cancer cells through reactive oxygen species-mediated mitochondrial damage

Kim

Lee

Kim

et al. 2016

Free Radical Biology and Medicine

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Section: Discussionmentioning

confidence: 99%

Sulfiredoxin inhibitor induces preferential death of cancer cells through reactive oxygen species-mediated mitochondrial damage

Kim

Lee

Kim

et al. 2016

Free Radical Biology and Medicine

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“…In the nucleus Nrf2 binds to the antioxidant response elements (ARE) of genes encoding antioxidant enzymes, as well as phase II detoxification enzymes of rapid induction and activation [56]. The main genes activated by Nrf2 include antioxidant enzymes such as HO-1 [58,59,60], NAD(P) H:quinone oxidoreductase 1 (NQO1) [60,61] and Prx1 [62,63]. It has been shown that in prostate cancer Nrf2 activation protects against OS, inducing radioresistance [64].…”

Section: Nuclear Factor (Erythoid-derived 2)-like 2 (Nrf2) Inducesmentioning

confidence: 99%

Reprogramming of Energy Metabolism in Response to Radiotherapy in Head and Neck Squamous Cell Carcinoma

Cruz-Gregorio

Martínez-Ramírez

Pedraza‐Chaverrí

et al. 2019

Cancers

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Head and neck cancer (HNC) is the sixth cause of cancer-related death worldwide. Head and neck squamous cells carcinoma (HNSCC) is the most frequent subtype of HNC. The development of HNSCC is associated to alcohol consumption, smoking or infection by high-risk human Papillomavirus (HR-HPV). Although the incidence of cancers associated with alcohol and tobacco has diminished, HNSCC associated with HR-HPV has significantly increased in recent years. However, HPV-positive HNSCC responds well to treatment, which includes surgery followed by radiation or chemoradiation therapy. Radiation therapy (RT) is based on ionizing radiation (IR) changing cell physiology. IR can directly interact with deoxyribonucleic acid (DNA) or produce reactive oxygen and nitrogen species (RONS), provoking DNA damage. When DNA damage is not repaired, programmed cell death (apoptosis and/or autophagy) is induced. However, cancer cells can acquire resistance to IR avoiding cell death, where reprogramming of energy metabolism has a critical role and is intimately connected with hypoxia, mitochondrial physiology, oxidative stress (OS) and autophagy. This review is focused on the reprogramming of energy metabolism in response to RT in HPV-positive and HPV-negative HNSCC, showing their differences in cellular metabolism management and the probable direction of treatments for each subtype of HNSCC.

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“…As mentioned above, PRDX1 is a potential target for cancer radiotherapy and/or chemotherapy. Several studies have suggested that anticancer molecules/gene reverse radioresistance through targeting PRDX1 on human lung cancer [88][89][90]. Vitamin K3 (vitK3) is a synthetic naphthoquinone exhibiting significant anticancer activity against multiple human cancers both in vitro and in vivo [91][92][93], and its major anticancer mechanism is depended on the generation of ROS [94,95].…”

Section: Prdx1 and Lung Cancermentioning

confidence: 99%

Peroxiredoxin 1 – an antioxidant enzyme in cancer

Ding

Fan

2016

J Cellular Molecular Medi

160

131

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Peroxiredoxins (PRDXs), a ubiquitous family of redox‐regulating proteins, are reported of potential to eliminate various reactive oxygen species (ROS). As a major member of the antioxidant enzymes, PRDX1 can become easily over‐oxidized on its catalytically active cysteine induced by a variety of stimuli in vitro and in vivo. In nucleus, oligomeric PRDX1 directly associates with p53 or transcription factors such as c‐Myc, NF‐κB and AR, and thus affects their bioactivities upon gene regulation, which in turn induces or suppresses cell death. Additionally, PRDX1 in cytoplasm has anti‐apoptotic potential through direct or indirect interactions with several ROS‐dependent (redox regulation) effectors, including ASK1, p66Shc, GSTpi/JNK and c‐Abl kinase. PRDX1 is proven to be a versatile molecule regulating cell growth, differentiation and apoptosis. Recent studies have found that PRDX1 and/or PRDX1‐regulated ROS‐dependent signalling pathways play an important role in the progression and metastasis of human tumours, particularly in breast, oesophageal and lung cancers. In this paper, we review the structure, effector functions of PRDX1, its role in cancer and the pivotal role of ROS in anticancer treatment.

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Downregulation of Peroxiredoxin I by a Novel Fully Human Phage Display Recombinant Antibody Induces Apoptosis and Enhances Radiation Sensitization in A549 Lung Carcinoma Cells

Abstract: These results suggested that Prx I scFv could become a new therapy candidate for lung cancer radiotherapy.

Cited by 11 publications

References 31 publications

Sulfiredoxin inhibitor induces preferential death of cancer cells through reactive oxygen species-mediated mitochondrial damage

Sulfiredoxin inhibitor induces preferential death of cancer cells through reactive oxygen species-mediated mitochondrial damage

Reprogramming of Energy Metabolism in Response to Radiotherapy in Head and Neck Squamous Cell Carcinoma

Peroxiredoxin 1 – an antioxidant enzyme in cancer

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