Reactive oxygen species (ROS) and cancer: Role of antioxidative nutraceuticals

Prasad, Sahdeo; Gupta, Subash C.; Tyagi, Amit

doi:10.1016/j.canlet.2016.03.042

Cited by 793 publications

(542 citation statements)

References 130 publications

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“…ROS are a double-edged sword; low to intermediate levels of ROS production may promote tumor initiation and progression, while excessive ROS can restrain cell viability, promote cell apoptosis, induce cell autophagy, and even trigger cell death. ROS induction currently has become a focus for anti-cancer drug design and application [29]. Here, increased ROS generation was detected when cells were cultured in a high glucose medium, which may account for the enhanced invasive ability.…”

Section: Discussionmentioning

confidence: 88%

Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of Pancreatic Cancer via AMPK Dependent Signaling

Chen

Jiang

Zhou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Sulforaphane (SFN) is known for its potent bioactive properties, such as anti-inflammatory and anti-tumor effects. However, its anti-tumor effect on pancreatic cancer is still poorly understood. In the present study, we explored the therapeutic potential of SFN for pancreatic cancer and disclosed the underlying mechanism. Methods: Panc-1 and MiaPaca-2 cell lines were used in vitro. The biological function of SFN in pancreatic cancer was measured using EdU staining, colony formation, apoptosis, migration and invasion assays. Reactive oxygen species (ROS) production was measured using 2’-7’-Dichlorofluorescein diacetate (DCF-DA) fluorometric analysis. Western blotting and immunofluorescence were used to measure the protein levels of p-AMPK and epithelial-mesenchymal transition (EMT) pathway-related proteins, and cellular translocation of nuclear factor erythroid 2-related factor 2 (Nrf2). Nude mice and transgenic pancreatic cancer mouse model were used to measure the therapeutic potential of SFN on pancreatic cancer. Results: SFN can inhibit pancreatic cancer cell growth， promote apoptosis, curb colony formation and temper the migratory and invasion ability of pancreatic cancer cells. Mechanistically, excessive ROS production induced by SFN activated AMPK signaling and promoted the translocation of Nrf2, resulting in cell viability inhibition of pancreatic cancer. Pretreatment with compound C, a small molecular inhibitor of AMPK signaling, reversed the subcellular translocation of Nrf2 and rescued cell invasion ability. With nude mice and pancreatic cancer transgenic mouse, we identified SFN could inhibit tumor progression, with smaller tumor size and slower tumor progression in SFN treatment group. Conclusion: Our study not only elucidates the mechanism of SFN-induced inhibition of pancreatic cancer in both normal and high glucose condition, but also testifies the dual-role of ROS in pancreatic cancer progression. Collectively, our research suggests that SFN may serve as a potential therapeutic choice for pancreatic cancer.

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Section: Discussionmentioning

confidence: 88%

Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of Pancreatic Cancer via AMPK Dependent Signaling

Chen

Jiang

Zhou

et al. 2018

Cell Physiol Biochem

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“…These rises in oxidative signaling have been implicated in the advancement of a variety of cancer types [161]. Moreover, ROS have been proposed to be involved in cancer initiation (as summarized above) as well as in malignant transformation (as summarized below) and in resistance to chemotherapies.…”

Section: Melatonin and Cancer Progressionmentioning

confidence: 99%

Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis

Reíter

Rosales-Corral

Tan

et al. 2017

IJMS

376

368

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There is highly credible evidence that melatonin mitigates cancer at the initiation, progression and metastasis phases. In many cases, the molecular mechanisms underpinning these inhibitory actions have been proposed. What is rather perplexing, however, is the large number of processes by which melatonin reportedly restrains cancer development and growth. These diverse actions suggest that what is being observed are merely epiphenomena of an underlying more fundamental action of melatonin that remains to be disclosed. Some of the arresting actions of melatonin on cancer are clearly membrane receptor-mediated while others are membrane receptor-independent and involve direct intracellular actions of this ubiquitously-distributed molecule. While the emphasis of melatonin/cancer research has been on the role of the indoleamine in restraining breast cancer, this is changing quickly with many cancer types having been shown to be susceptible to inhibition by melatonin. There are several facets of this research which could have immediate applications at the clinical level. Many studies have shown that melatonin’s co-administration improves the sensitivity of cancers to inhibition by conventional drugs. Even more important are the findings that melatonin renders cancers previously totally resistant to treatment sensitive to these same therapies. Melatonin also inhibits molecular processes associated with metastasis by limiting the entrance of cancer cells into the vascular system and preventing them from establishing secondary growths at distant sites. This is of particular importance since cancer metastasis often significantly contributes to death of the patient. Another area that deserves additional consideration is related to the capacity of melatonin in reducing the toxic consequences of anti-cancer drugs while increasing their efficacy. Although this information has been available for more than a decade, it has not been adequately exploited at the clinical level. Even if the only beneficial actions of melatonin in cancer patients are its ability to attenuate acute and long-term drug toxicity, melatonin should be used to improve the physical wellbeing of the patients. The experimental findings, however, suggest that the advantages of using melatonin as a co-treatment with conventional cancer therapies would far exceed improvements in the wellbeing of the patients.

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“…Guo et al reported that the induction of mitophagy in macrophages prevents the progression of colitis-associated cancer (22). Moreover, tumorigenesis and metastasis are also promoted by mitochondrial reactive oxygen species (ROS) (23). According to Chourasia et al, BNIP3 loss, and ensuing defects in mitophagy, leads to ROS production and mammary neoplastic progression to metastasis (4).…”

Section: Biological Role Of Mitophagymentioning

confidence: 99%

Dual Role of Mitophagy in Cancer Drug Resistance

Yan

2018

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Reactive oxygen species (ROS) and cancer: Role of antioxidative nutraceuticals

Cited by 793 publications

References 130 publications

Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of Pancreatic Cancer via AMPK Dependent Signaling

Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of Pancreatic Cancer via AMPK Dependent Signaling

Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis

Dual Role of Mitophagy in Cancer Drug Resistance

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