Reductive Stress, Bioactive Compounds, Redox-Active Metals, and Dormant Tumor Cell Biology to Develop Redox-Based Tools for the Treatment of Cancer

Quiles, José L.; Sánchez-González, Cristina; Vera-Ramírez, Laura; Giampieri, Francesca; Navarro-Hortal, María D.; Xiao, Jianbo; Llopis, Juan; Battino, Maurizio; Varela-López, Alfonso

doi:10.1089/ars.2020.8051

Cited by 28 publications

(14 citation statements)

References 157 publications

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“…This study describes, for the first time, that POTs can affect aquaporin function and lead to the inhibition of cancer cell migration. POMs are potential candidates for anticancer drugs in the future since several types of POMs showed anticancer activities at various concentrations ranging from nM to µM [3,9,13,[37][38][39][40][41][42][43][44]. In fact, in most cases, when compared with already approved anticancer drugs, POMs were more efficient.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, some POMs are also understood to interfere with mitochondria function and DNA, while others can exert an immunomodulatory activity [9,10]. As the incidence of cancer is increasing every year all over the world, along with the growing resistance effect and high toxicity of chemotherapeutic agents, some researchers chose POMs as alternative anti-tumor substances with promising results in suppressing tumor growth [3,9,[11][12][13].…”

Section: Introductionmentioning

confidence: 99%

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The Aquaporin-3-Inhibiting Potential of Polyoxotungstates

Pimpão

Silva

Mósca

et al. 2020

IJMS

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Polyoxometalates (POMs) are of increasing interest due to their proven anticancer activities. Aquaporins (AQPs) were found to be overexpressed in tumors bringing particular attention to their inhibitors as anticancer drugs. Herein, we report for the first time the ability of polyoxotungstates (POTs), such as of Wells–Dawson P2W18, P2W12, and P2W15, and Preyssler P5W30 structures, to affect aquaporin-3 (AQP3) activity and impair melanoma cell migration. The tested POTs were revealed to inhibit AQP3 function with different effects, with P2W18, P2W12, and P5W30 being the most potent (50% inhibitory concentration (IC50) = 0.8, 2.8, and 3.2 µM), and P2W15 being the weakest (IC50 > 100 µM). The selectivity of P2W18 toward AQP3 was confirmed in yeast cells transformed with human aquaglyceroporins. The effect of P2W12 and P2W18 on melanoma cells that highly express AQP3 revealed an impairment of cell migration between 55% and 65% after 24 h, indicating that the anticancer properties of these compounds may in part be due to the blockage of AQP3-mediated permeability. Altogether, our data revealed that P2W18 strongly affects AQP3 activity and cancer cell growth, unveiling its potential as an anticancer drug against tumors where AQP3 is highly expressed.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Aquaporin-3-Inhibiting Potential of Polyoxotungstates

Pimpão

Silva

Mósca

et al. 2020

IJMS

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“…They may reactivate and regrow after a long period of time and are considered as a vital reason for the recurrence of cancer. Prior studies have shown that existence of dormant cells ensures metastasis of cancer cells and is correlated with poor prognosis [483][484][485][486]. To date, there is no experiment about the relationship between CP, EMT, and dormant cells.…”

Section: Conclusion and Remarksmentioning

confidence: 99%

Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance

Ashrafizadeh

Zarrabi

Hushmandi

et al. 2020

IJMS

191

103

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Therapy resistance is a characteristic of cancer cells that significantly reduces the effectiveness of drugs. Despite the popularity of cisplatin (CP) as a chemotherapeutic agent, which is widely used in the treatment of various types of cancer, resistance of cancer cells to CP chemotherapy has been extensively observed. Among various reported mechanism(s), the epithelial–mesenchymal transition (EMT) process can significantly contribute to chemoresistance by converting the motionless epithelial cells into mobile mesenchymal cells and altering cell–cell adhesion as well as the cellular extracellular matrix, leading to invasion of tumor cells. By analyzing the impact of the different molecular pathways such as microRNAs, long non-coding RNAs, nuclear factor-κB (NF-ĸB), phosphoinositide 3-kinase-related protein kinase (PI3K)/Akt, mammalian target rapamycin (mTOR), and Wnt, which play an important role in resistance exhibited to CP therapy, we first give an introduction about the EMT mechanism and its role in drug resistance. We then focus specifically on the molecular pathways involved in drug resistance and the pharmacological strategies that can be used to mitigate this resistance. Overall, we highlight the various targeted signaling pathways that could be considered in future studies to pave the way for the inhibition of EMT-mediated resistance displayed by tumor cells in response to CP exposure.

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“…Altogether, these effects directly impaired the inflammatory response, inducing a pro-inflammatory state [25,62]. Oxidative stress arises and is maintained due to the increase in mitochondrial ROS production and inefficient (or absence) of enough AOX levels, resulting in an imbalance of the cellular redox state [64,65].…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 99%

Diabetes Mellitus and Periodontitis Share Intracellular Disorders as the Main Meeting Point

Portes

Bullón

Quiles

et al. 2021

Cells

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Diabetes and periodontitis are two of the most prevalent diseases worldwide that negatively impact the quality of life of the individual suffering from them. They are part of the chronic inflammatory disease group or, as recently mentioned, non-communicable diseases, with inflammation being the meeting point among them. Inflammation hitherto includes vascular and tissue changes, but new technologies provide data at the intracellular level that could explain how the cells respond to the aggression more clearly. This review aims to emphasize the molecular pathophysiological mechanisms in patients with type 2 diabetes mellitus and periodontitis, which are marked by different impaired central regulators including mitochondrial dysfunction, impaired immune system and autophagy pathways, oxidative stress, and the crosstalk between adenosine monophosphate-activated protein kinase (AMPK) and the renin-angiotensin system (RAS). All of them are the shared background behind both diseases that could explain its relationship. These should be taken in consideration if we would like to improve the treatment outcomes. Currently, the main treatment strategies in diabetes try to reduce glycemia index as the most important aspect, and in periodontitis try to reduce the presence of oral bacteria. We propose to add to the therapeutic guidelines the handling of all the intracellular disorders to try to obtain better treatment success.

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Reductive Stress, Bioactive Compounds, Redox-Active Metals, and Dormant Tumor Cell Biology to Develop Redox-Based Tools for the Treatment of Cancer

Cited by 28 publications

References 157 publications

The Aquaporin-3-Inhibiting Potential of Polyoxotungstates

The Aquaporin-3-Inhibiting Potential of Polyoxotungstates

Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance

Diabetes Mellitus and Periodontitis Share Intracellular Disorders as the Main Meeting Point

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