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Review
. 2022 Sep 29:10:1005910.
doi: 10.3389/fcell.2022.1005910. eCollection 2022.

Recent updates on anticancer mechanisms of polyphenols

Eshita Sharma  1 , Dharam Chand Attri  2 , Priyanka Sati  3 , Praveen Dhyani  4 , Agnieszka Szopa  5 , Javad Sharifi-Rad  6 , Christophe Hano  7 , Daniela Calina  8 , William C Cho  9
Affiliations
Review

Recent updates on anticancer mechanisms of polyphenols

Eshita Sharma et al. Front Cell Dev Biol. .

Abstract

In today's scenario, when cancer cases are increasing rapidly, anticancer herbal compounds become imperative. Studies on the molecular mechanisms of action of polyphenols published in specialized databases such as Web of Science, Pubmed/Medline, Google Scholar, and Science Direct were used as sources of information for this review. Natural polyphenols provide established efficacy against chemically induced tumor growth with fewer side effects. They can sensitize cells to various therapies and increase the effectiveness of biotherapy. Further pharmacological translational research and clinical trials are needed to evaluate theirs in vivo efficacy, possible side effects and toxicity. Polyphenols can be used to design a potential treatment in conjunction with existing cancer drug regimens such as chemotherapy and radiotherapy.

Keywords: anticancer molecular mechanisms; cancer; invasion; migration; pharmacology; phytochemicals; polyphenols.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Chemical structures of most representative polyphenols employed as anticancer agents.
FIGURE 2
FIGURE 2
Potential molecular targets and signaling pathways for the antitumor effect of polyphenols. Symbols: ↑increase, ↓decrease. Abbreviations: ADAM17, ADAM metallopeptidase domain 17; Akt/mTOR, protein kinase B/mammalian target of rapamycin; AMPK, adenosine monophosphate-activated protein kinase; BAD, Bcl-2 antagonist of cell death; Bax, Bcl2-Associated X Protein; Bcl-2, B-cell leukemia/lymphoma 2 protein; Bcl-xL, B-cell lymphoma-extra large; c/ebp-α, CCAAT/enhancer-binding protein-alpha; DR-5, death receptor 5; EGFR, epidermal growth factor receptor; ERK/MSK, extracellular signal-regulated kinase/mitogen- and stress-activated kinase 1; Her2/Neu, human epidermal growth factor receptor 2/neutrophills; HIF-1-alpha, hypoxia-inducible factor 1-alpha; IGFBP-5, insulin-like growth factor-binding protein-5; hTERT, human telomerase reverse transcriptase; miR, microRNA; MMP, matrix metalloproteinase; MnK-1, a family of serine/threonine kinases; mRNA, messenger ribonucleic acid; mTOR, mammalian target of rapamycin; mTORC2, mTOR Complex 2; NF-κB, nuclear factor kappa B; Nrf1, nuclear respiratory factor 1; PI3K: phosphatidylinositol 3-kinase; pro-NAG-1, pro-nonsteroidal anti-inflammatory drug-activated gene-1; pTEN, phosphatase and TENsin homolog deleted on chromosome 10; PTK, protein tyrosine kinase; TGF-β1, transforming growth factor-β1; TRAIL, tumor-necrosis factor related apoptosis-inducing ligand; UGT1A, UDP glucuronosyltransferase 1 family; VEGF, vascular endothelial growth factor receptor; Wnt, wingless-related integration site.
See this image and copyright information in PMC

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