Resveratrol in breast cancer treatment: from cellular effects to molecular mechanisms of action

Behroozaghdam, Mitra; Dehghani, Maryam; Zabolian, Amirhossein; Kamali, Davood; Javanshir, Salar; Sadi, Farzaneh Hasani; Hashemi, Mehrdad; Tabari, Teimour; Rashidi, Mohsen; Mirzaei, Sepideh; Zarepour, Atefeh; Zarrabi, Ali; Greef, Danielle De; Bishayee, Anupam

doi:10.1007/s00018-022-04551-4

Cited by 34 publications

(26 citation statements)

References 271 publications

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“…These results indicate the cytotoxic effectiveness of compound RV in suppressing the growth of MCF7 cells at micromolar range. Our findings suggest that the compound RV has the potential to inhibit the proliferation of cancerous cells and resonate with the previous reports of cytotoxicity of RV on similar or other cancer cells [56][57][58][59].…”

Section: Cell Proliferation Assaysupporting

confidence: 92%

Repurposing Resveratrol: A Novel Approach to Inhibit MTH1 for Effective Breast Cancer Therapy

Taiyab,

Haider,

Choudhury

et al. 2024

Preprint

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The increased metabolic activity in cancer cells often leads to higher levels of reactive oxygen species (ROS) compared to normal cells, which can cause damage to cellular components, including DNA. Cancer cells rely on MTH1 to maintain their DNA integrity and cellular function to counteract this damage. MTH1 is critical in sanitizing oxidized nucleotide pools by removing damaged nucleotides. Inhibition of MTH1 disrupts this repair process, leading to increased DNA damage and cell death in cancer cells. In this study, we present resveratrol (RV) as a potential MTH1 inhibitor. Docking and MD Simulations illustrated the effective binding of RV to the active site of the MTH1 protein, forming a notably stable complex. The fluorescence binding studies estimated a high binding affinity of RV with MTH1 (Ka − 6.2 x 105), inhibiting MTH1 activity with IC50 20.4µM. The inhibitory effects of RV on the proliferation of breast cancer cells revealed significant inhibition in cell growth, leading to apoptosis. RV significantly increases ROS production, inducing considerable oxidative stress and ultimately resulting in cell death. Our study offers a rationale for evaluating RV as an MTH1 inhibitor for potential anti-cancer therapy, particularly in breast cancer.

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Section: Cell Proliferation Assaysupporting

confidence: 92%

Repurposing Resveratrol: A Novel Approach to Inhibit MTH1 for Effective Breast Cancer Therapy

Taiyab,

Haider,

Choudhury

et al. 2024

Preprint

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“…Resveratrol is a natural phytoalexin that regulates the cascade of STAT signaling and has the potential to mitigate breast cancer progression [96]. Studies have been conducted in vitro that showed the target of Resveratrol is STAT3 protein [97]. Resveratrol triggers a stepwise inhibition cascade involving Src tyrosine kinase and STAT3 proteins.…”

Section: Potential Treatments Targeting Cell‐intrinsic Pathways Media...mentioning

confidence: 99%

Unraveling the dangerous duet between cancer cell plasticity and drug resistance

Chatterjee,

Pulipaka,

Subbalakshmi

et al. 2023

Comp Sys Onco

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Cancer cell plasticity is the ability of tumor cells to switch phenotypes and is one of the predominant requisites of cancer cells capable of undergoing metastasis. Cancer cell plasticity is also recognized as one of the major contributors to intratumoral heterogeneity, a critical factor underlying the progression of malignant tumors, which is known to modify tumor response and induce resistance against various modes of therapy, thus posing a barrier to efficient cancer management. Cancer cell plasticity is acquired by the subversion of cell signaling pathways like mitogen‐activated protein kinase pathway, phosphoinositide‐3‐kinase, signal transducer and activator of transcription 3, Wnt, Hedgehog and Notch as well as cellular programs such as epithelial to mesenchymal transition and phenotypic plasticity. This complex phenomenon has been studied in many cancer types like pancreatic cancer, colon cancer and breast cancer. This review will explore the current understanding we have in breast cancer on the intrinsic molecular mechanisms of cancer cell plasticity and the resistance to various types of cancer therapy that arise as a result of plasticity. We conclude by exploring the potential novel therapies that specifically target the pathways leading to plasticity and can be leveraged to treat patients living with the disease.

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“…Resveratrol (RES) is a natural non-flavonoid polyphenolic compound isolated from natural plants such as grapes, peanuts, blueberries, bilberries, cranberries, and certain medicinal herbs [ 8 ]. RES exhibits diverse pharmacological actions such as cardioprotective, nephroprotective, hepatoprotective, neuroprotective, anti-oxidant, anti-inflammatory, anti-osteoporosis, anti-diabetic, anti-obesity, anti-atherosclerosis, anti-aging, and anti-tumor properties through regulating a broad spectrum of molecular targets and signaling pathways [ 11 , 12 ]. RES has been widely available as an over-the-counter nutritional supplement with an array of alleged salutary effects [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Uncovering the mechanism of resveratrol in the treatment of diabetic kidney disease based on network pharmacology, molecular docking, and experimental validation

Chen

et al. 2023

J Transl Med

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Background Diabetic kidney disease (DKD) has been the leading cause of chronic kidney disease in developed countries. Evidence of the benefits of resveratrol (RES) for the treatment of DKD is accumulating. However, comprehensive therapeutic targets and underlying mechanisms through which RES exerts its effects against DKD are limited. Methods Drug targets of RES were obtained from Drugbank and SwissTargetPrediction Databases. Disease targets of DKD were obtained from DisGeNET, Genecards, and Therapeutic Target Database. Therapeutic targets for RES against DKD were identified by intersecting the drug targets and disease targets. GO functional enrichment analysis, KEGG pathway analysis, and disease association analysis were performed using the DAVID database and visualized by Cytoscape software. Molecular docking validation of the binding capacity between RES and targets was performed by UCSF Chimera software and SwissDock webserver. The high glucose (HG)-induced podocyte injury model, RT-qPCR, and western blot were used to verify the reliability of the effects of RES on target proteins. Results After the intersection of the 86 drug targets and 566 disease targets, 25 therapeutic targets for RES against DKD were obtained. And the target proteins were classified into 6 functional categories. A total of 11 cellular components terms and 27 diseases, and the top 20 enriched biological processes, molecular functions, and KEGG pathways potentially involved in the RES action against DKD were recorded. Molecular docking studies showed that RES had a strong binding affinity toward PPARA, ESR1, SLC2A1, SHBG, AR, AKR1B1, PPARG, IGF1R, RELA, PIK3CA, MMP9, AKT1, INSR, MMP2, TTR, and CYP2C9 domains. The HG-induced podocyte injury model was successfully constructed and validated by RT-qPCR and western blot. RES treatment was able to reverse the abnormal gene expression of PPARA, SHBG, AKR1B1, PPARG, IGF1R, MMP9, AKT1, and INSR. Conclusions RES may target PPARA, SHBG, AKR1B1, PPARG, IGF1R, MMP9, AKT1, and INSR domains to act as a therapeutic agent for DKD. These findings comprehensively reveal the potential therapeutic targets for RES against DKD and provide theoretical bases for the clinical application of RES in the treatment of DKD.

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Resveratrol in breast cancer treatment: from cellular effects to molecular mechanisms of action

Cited by 34 publications

References 271 publications

Repurposing Resveratrol: A Novel Approach to Inhibit MTH1 for Effective Breast Cancer Therapy

Repurposing Resveratrol: A Novel Approach to Inhibit MTH1 for Effective Breast Cancer Therapy

Unraveling the dangerous duet between cancer cell plasticity and drug resistance

Uncovering the mechanism of resveratrol in the treatment of diabetic kidney disease based on network pharmacology, molecular docking, and experimental validation

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