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Phytochemicals and Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 5839

Special Issue Editor


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Guest Editor
Department of Internal Medicine, Institute of Health Sciences, Gyeongsang National University Hospital, Gyeongsang National University School of Medicine, Jinju 660-702, Republic of Korea
Interests: tumor suppressor gene; oncogene; phytochemials; targeted approach; cell death; molecular mechanisms; cancer therapy
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Special Issue Information

Dear Colleagues,

Cancer is a deadly disorder which may not only take the life of the patient, but can also destroy the lives of the family and friends who act as their caregivers. This disease starts with accumulation of genetic changes in cells that affect cell growth and survival. The cancer cell acquires the ability to grow uncontrollably, invade normal tissue, and then spread into a nearby or distant organ. The cells can then destroy multiple organs and finally take the person’s life.

Phytochemicals are chemicals of plant origin. They generally help the plant resist competitors, pathogens, or predators. Evidence suggests that some of them showed anticancer effects in terms of proliferation, survival, invasion, and metastasis of cancer. We also know that phytochemicals are very important resources for anticancer drug development.

This Special Issue is dedicated to original research articles, short communications, and reviews related to the following topics, which cover the latest findings on the role of phytochemicals in the prevention and treatment of cancer. 

1. The role of phytochemicals in carcinogenesis.
2. The role of phytochemicals in the chemoprevention.
3. The role of phytochemicals in the cancer treatment as anticancer agents.
4. The role of phytochemicals in the cancer treatment as an enhancer of a certain chemotherapeutic agents.
5. Characterized bioactive components from a natural plant extract showing anticancer effects.

Dr. Won Sup Lee
Guest Editor

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Keywords

  • cancer
  • phytochemicals
  • chemoprevention
  • anticancer effects
  • signaling mechanisms

Published Papers (2 papers)

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Research

18 pages, 4358 KiB  
Article
β-Lapachone Exerts Anticancer Effects by Downregulating p53, Lys-Acetylated Proteins, TrkA, p38 MAPK, SOD1, Caspase-2, CD44 and NPM in Oxaliplatin-Resistant HCT116 Colorectal Cancer Cells
by Eun Joo Jung, Hye Jung Kim, Sung Chul Shin, Gon Sup Kim, Jin-Myung Jung, Soon Chan Hong, Choong Won Kim and Won Sup Lee
Int. J. Mol. Sci. 2023, 24(12), 9867; https://doi.org/10.3390/ijms24129867 - 7 Jun 2023
Cited by 3 | Viewed by 1866
Abstract
β-lapachone (β-Lap), a topoisomerase inhibitor, is a naturally occurring ortho-naphthoquinone phytochemical and is involved in drug resistance mechanisms. Oxaliplatin (OxPt) is a commonly used chemotherapeutic drug for metastatic colorectal cancer, and OxPt-induced drug resistance remains to be solved to increase chances of [...] Read more.
β-lapachone (β-Lap), a topoisomerase inhibitor, is a naturally occurring ortho-naphthoquinone phytochemical and is involved in drug resistance mechanisms. Oxaliplatin (OxPt) is a commonly used chemotherapeutic drug for metastatic colorectal cancer, and OxPt-induced drug resistance remains to be solved to increase chances of successful therapy. To reveal the novel role of β-Lap associated with OxPt resistance, 5 μM OxPt-resistant HCT116 cells (HCT116-OxPt-R) were generated and characterized via hematoxylin staining, a CCK-8 assay and Western blot analysis. HCT116-OxPt-R cells were shown to have OxPt-specific resistance, increased aggresomes, upregulated p53 and downregulated caspase-9 and XIAP. Through signaling explorer antibody array, nucleophosmin (NPM), CD37, Nkx-2.5, SOD1, H2B, calreticulin, p38 MAPK, caspase-2, cadherin-9, MMP23B, ACOT2, Lys-acetylated proteins, COL3A1, TrkA, MPS-1, CD44, ITGA5, claudin-3, parkin and ACTG2 were identified as OxPt-R-related proteins due to a more than two-fold alteration in protein status. Gene ontology analysis suggested that TrkA, Nkx-2.5 and SOD1 were related to certain aggresomes produced in HCT116-OxPt-R cells. Moreover, β-Lap exerted more cytotoxicity and morphological changes in HCT116-OxPt-R cells than in HCT116 cells through the downregulation of p53, Lys-acetylated proteins, TrkA, p38 MAPK, SOD1, caspase-2, CD44 and NPM. Our results indicate that β-Lap could be used as an alternative drug to overcome the upregulated p53-containing OxPt-R caused by various OxPt-containing chemotherapies. Full article
(This article belongs to the Special Issue Phytochemicals and Cancer)
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15 pages, 5576 KiB  
Article
Identification of Growth Factors, Cytokines and Mediators Regulated by Artemisia annua L. Polyphenols (pKAL) in HCT116 Colorectal Cancer Cells: TGF-β1 and NGF-β Attenuate pKAL-Induced Anticancer Effects via NF-κB p65 Upregulation
by Eun Joo Jung, Anjugam Paramanantham, Hye Jung Kim, Sung Chul Shin, Gon Sup Kim, Jin-Myung Jung, Soon Chan Hong, Ky Hyun Chung, Choong Won Kim and Won Sup Lee
Int. J. Mol. Sci. 2022, 23(3), 1598; https://doi.org/10.3390/ijms23031598 - 29 Jan 2022
Cited by 6 | Viewed by 2807
Abstract
The anticancer effects of natural phytochemicals are relevant to the modulation of cytokine signaling pathways in various cancer cells with stem-like properties as well as immune cells. The aim of this study was to elucidate a novel anticancer mechanism of Artemisia annua L. [...] Read more.
The anticancer effects of natural phytochemicals are relevant to the modulation of cytokine signaling pathways in various cancer cells with stem-like properties as well as immune cells. The aim of this study was to elucidate a novel anticancer mechanism of Artemisia annua L. polyphenols (pKAL) involved in the regulation of growth factors, cytokines and mediators in stem-like HCT116 colorectal cancer cells. Through RayBiotech human L-1000 antibody array and bioinformatics analysis, we show here that pKAL-induced anticancer effects are associated with downregulation of growth factor and cytokine signaling proteins including TGFA, FGF16, PDGFC, CCL28, CXCR3, IRF6 and SMAD1. Notably, we found that TGF-β signaling proteins such as GDF10, ENG and TGFBR2 and well-known survival proteins such as NGF-β, VEGFD and insulin were significantly upregulated by pKAL. Moreover, the results of hematoxylin staining, cell viability assay and Western blot analysis demonstrated that TGF-β1 and NGF-β attenuated pKAL-induced anticancer effects by inhibiting pKAL-induced downregulation of caspase-8, NF-κB p65 and cyclin D1. These results suggest that certain survival mediators may be activated by pKAL through the TGF-β1 and NGF-β signaling pathways during pKAL-induced cell death and thus, strategies to inhibit the survival signaling are inevitably required for more effective anticancer effects of pKAL. Full article
(This article belongs to the Special Issue Phytochemicals and Cancer)
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