Microcystins-LR induced apoptosis via S-nitrosylation of GAPDH in colorectal cancer cells

Li, Keyi; Huang, Mengqiu; Xu, Pengfei; Wang, Meng; Ye, Shuangyan; Wang, Qianli; Zeng, Sisi; Chen, Xi; Gao, Wenwen; Chen, Jianping; Zhang, Qianbing; Zhong, Zhuo; Sun, Yang; Liu, Qiuzhen

doi:10.1016/j.ecoenv.2019.110096

Cited by 17 publications

(10 citation statements)

References 35 publications

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“…To investigate the impact of MC-LR on CRC cell proliferation, a suitable concentration of MC-LR needs to be selected. Several studies have used 25 or 50 nM MC-LR to treat CRC cells (14,15,29). For example, Miao et al (14) It has been reported that MC-LR could accelerate CRC cell migration and metastasis (14,15).…”

Section: Discussionmentioning

confidence: 99%

Microcystin‑leucine arginine promotes colorectal cancer cell proliferation by activating the PI3K/Akt/Wnt/β‑catenin pathway

Tang

Zhang

et al. 2022

Oncol Rep

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Microcystin-leucine arginine (MC-LR) is an environmental toxin produced by cyanobacteria and is considered to be a potent carcinogen. However, to the best of our knowledge, the effect of MC-LR on colorectal cancer (CRC) cell proliferation has never been studied. The aim of the present study was to investigate the effect of MC-LR on CRC cell proliferation and the underlying mechanisms. Firstly, a Cell Counting Kit-8 (CCK-8) assay was conducted to determine cell viability at different concentrations, and 50 nM MC-LR was chosen for further study.

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Section: Discussionmentioning

confidence: 99%

Microcystin‑leucine arginine promotes colorectal cancer cell proliferation by activating the PI3K/Akt/Wnt/β‑catenin pathway

Tang

Zhang

et al. 2022

Oncol Rep

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“…The stabilization of GAPDH in the cytoplasm is critical for mutant p53 induced antiapoptosis. A recent study by Li et al showed that GAPDH's translocation into the nucleus increases transcription of p53 gene, providing additional evidence on interplay between p53 and GAPDH in regulating cellular apoptosis [175].…”

Section: Glycolysismentioning

confidence: 93%

Reactive Oxygen Species, Metabolic Plasticity, and Drug Resistance in Cancer

Bhardwaj

2020

IJMS

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The metabolic abnormality observed in tumors is characterized by the dependence of cancer cells on glycolysis for their energy requirements. Cancer cells also exhibit a high level of reactive oxygen species (ROS), largely due to the alteration of cellular bioenergetics. A highly coordinated interplay between tumor energetics and ROS generates a powerful phenotype that provides the tumor cells with proliferative, antiapoptotic, and overall aggressive characteristics. In this review article, we summarize the literature on how ROS impacts energy metabolism by regulating key metabolic enzymes and how metabolic pathways e.g., glycolysis, PPP, and the TCA cycle reciprocally affect the generation and maintenance of ROS homeostasis. Lastly, we discuss how metabolic adaptation in cancer influences the tumor’s response to chemotherapeutic drugs. Though attempts of targeting tumor energetics have shown promising preclinical outcomes, the clinical benefits are yet to be fully achieved. A better understanding of the interaction between metabolic abnormalities and involvement of ROS under the chemo-induced stress will help develop new strategies and personalized approaches to improve the therapeutic efficiency in cancer patients.

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“…S-nitrosylation is a dynamic bidirectional process, and the relative balance of nitrosylated and de-nitrosylated proteins can serve as a biofeedback mechanism for physiological functions [30,31]. In the heart and vasculature, protein de-nitrysolation via S-nitrosoglutathione reductase (GSNO-R) regulates vascular tone and β adrenergic activity [31], the processes of S-nitrosylation and de-nitrosylation are important regulatory mechanisms for carcinogenesis and metastasis and may be responsible for ischemic episodes and more [32][33][34][35]. Importantly, hemoglobin is a key target of S-nitrosylation, whereby S-nitrosylated thiols participate in the allosteric shift that regulates the process of oxygen loading and unloading [36].…”

Section: No-mediated Post-translational Modificationsmentioning

confidence: 99%

Current Advances of Nitric Oxide in Cancer and Anticancer Therapeutics

et al. 2021

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Nitric oxide (NO) is a short-lived, ubiquitous signaling molecule that affects numerous critical functions in the body. There are markedly conflicting findings in the literature regarding the bimodal effects of NO in carcinogenesis and tumor progression, which has important consequences for treatment. Several preclinical and clinical studies have suggested that both pro- and antitumorigenic effects of NO depend on multiple aspects, including, but not limited to, tissue of generation, the level of production, the oxidative/reductive (redox) environment in which this radical is generated, the presence or absence of NO transduction elements, and the tumor microenvironment. Generally, there are four major categories of NO-based anticancer therapies: NO donors, phosphodiesterase inhibitors (PDE-i), soluble guanylyl cyclase (sGC) activators, and immunomodulators. Of these, NO donors are well studied, well characterized, and also the most promising. In this study, we review the current knowledge in this area, with an emphasis placed on the role of NO as an anticancer therapy and dysregulated molecular interactions during the evolution of cancer, highlighting the strategies that may aid in the targeting of cancer.

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Microcystins-LR induced apoptosis via S-nitrosylation of GAPDH in colorectal cancer cells

Cited by 17 publications

References 35 publications

Microcystin‑leucine arginine promotes colorectal cancer cell proliferation by activating the PI3K/Akt/Wnt/β‑catenin pathway

Microcystin‑leucine arginine promotes colorectal cancer cell proliferation by activating the PI3K/Akt/Wnt/β‑catenin pathway

Reactive Oxygen Species, Metabolic Plasticity, and Drug Resistance in Cancer

Current Advances of Nitric Oxide in Cancer and Anticancer Therapeutics

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