Effective Killing of Cancer Cells Through ROS-Mediated Mechanisms by AMRI-59 Targeting Peroxiredoxin I

Yang, Yan; Baek, Jin Young; Goo, Jail; Shin, Yeong Gil; Park, Jong Kuk; Jang, Ji Yong; Wang, Su Bin; Jeong, Woojin; Lee, Hwa Jeong; Um, Hong Duck; Lee, Sang Kook; Choi, Yongseok; Rhee, Sue Goo; Chang, Tong Shin

doi:10.1089/ars.2014.6187

Cited by 36 publications

(27 citation statements)

References 70 publications

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“…The mouse model studies have shown that Prx I deficiency induces various malignant tumors (Neumann et al, 2003) and aggravates the KRAS-induced spontaneous lung tumorigenesis (Park et al, 2013). However, the chemical inhibition of Prx I activity was shown to cause death of the lung carcinoma cells through in vitro culture and acute tumor xenograft (Yang et al, 2015). In this study, we demonstrate that Prx I is a residential nucleosomal protein that prevents the oxidative DNA damage.…”

Section: Prx I-dependent Apoptosis Regulationmentioning

confidence: 55%

Absence of Cytosolic 2-Cys Prx Subtypes I and II Exacerbates TNF-α-Induced Apoptosis via Different Routes

Lee

et al. 2019

Cell Reports

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Section: Prx I-dependent Apoptosis Regulationmentioning

confidence: 55%

Absence of Cytosolic 2-Cys Prx Subtypes I and II Exacerbates TNF-α-Induced Apoptosis via Different Routes

Lee

et al. 2019

Cell Reports

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“…31, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49 It is also well accepted that the efficacy of many anticancer therapies, including chemotherapeutics and radiotherapy, largely depends on their ability to induce ROS accumulation and evoke cell toxicity and death. 14, 50, 51, 52, 53, 54, 55, 56 The high levels of oxidative stress normally associated with malignant progression represent tumor-specific alteration that makes cancer cells vulnerable to further elevation of ROS and strongly dependent on their antioxidant defenses. Both extrinsic and intrinsic factors contribute to generate a persistent amount of high ROS levels in tumors.…”

Section: Ros Homeostasis and Redox Cofactors In Normal And Tumor Cellsmentioning

confidence: 99%

ROS homeostasis and metabolism: a dangerous liason in cancer cells

2016

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Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage and genomic instability, and ultimately, by reprogramming cancer cell metabolism. This review outlines the metabolic-dependent mechanisms that tumors engage in when faced with oxidative stress conditions that are critical for cancer progression by producing redox cofactors. In particular, we describe how the mitochondria has a key role in regulating the interplay between redox homeostasis and metabolism within tumor cells. Last, we will discuss the potential therapeutic use of agents that directly or indirectly block metabolism.

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“…Prdxs have been reported to be differentially expressed in human pancreatic cancer [7], Burkitt lymphoma [8], lung carcinoma [9], colorectal carcinoma [10], prostate cancer [11], myeloma [12], and leukemia [13]. Prdx2, a typical 2-Cys peroxiredoxin, has higher expression levels in tumorous colon tissues compared with the corresponding normal non-tumor tissues [14], and Prdx2 knockdown inhibits cell growth and stimulates apoptosis [10].…”

Section: Introductionmentioning

confidence: 99%

Peroxiredoxin 2 is essential for maintaining cancer stem cell-like phenotype through activation of Hedgehog signaling pathway in colon cancer

et al. 2016

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Cancer stem cells (CSCs) are a key target for reducing tumor growth, metastasis, and recurrence. Redox status is a critical factor in the maintenance of CSCs, and the antioxidant enzyme Peroxiredoxin 2 (Prdx2) plays an important role in the development of colon cancer. Therefore, we investigated the contribution of Prdx2 to the maintenance of stemness of colon CSCs. Here, we used short-hairpin RNAs and a Prdx2-overexpression vector to determine the effects of Prdx2. We demonstrated that knockdown of Prdx2 reduced the self-renewal and sphere formation and resulted in increased 5-FU-induced apoptosis in human colon CSCs. Prdx2 overexpression induced reversion of the self-renewal and sphere formation. Furthermore, the effects of Prdx2 resulted in an altered expression of stemness associated with the Hh/Gli1 signaling pathway. Finally, knockdown of Prdx2 in CD133+ cells reduced the volume of xenograft tumors in BALB/c-nu mice. Taken together, colon CSCs overexpress Prdx2, which promotes their stem cell properties via the Hh/Gli1 signaling pathway. The results suggest that Prdx2 may be an effective therapeutic target for the elimination of CSCs in colorectal cancer.

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Effective Killing of Cancer Cells Through ROS-Mediated Mechanisms by AMRI-59 Targeting Peroxiredoxin I

Abstract: Our results highlight a promising strategy for cancer therapy that preferentially eradicates cancer cells by targeting the PrxI-mediated redox-dependent survival pathways.

Cited by 36 publications

References 70 publications

Absence of Cytosolic 2-Cys Prx Subtypes I and II Exacerbates TNF-α-Induced Apoptosis via Different Routes

Absence of Cytosolic 2-Cys Prx Subtypes I and II Exacerbates TNF-α-Induced Apoptosis via Different Routes

ROS homeostasis and metabolism: a dangerous liason in cancer cells

Peroxiredoxin 2 is essential for maintaining cancer stem cell-like phenotype through activation of Hedgehog signaling pathway in colon cancer

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