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Natural Active Substances and Cancer

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Phytochemicals and Human Health".

Deadline for manuscript submissions: 15 July 2025 | Viewed by 501

Special Issue Editor


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Guest Editor
Department of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, 1-Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan
Interests: IL-8; CXCR4; cytokine; cancer stromal interaction; chemokine; angiogenesis; chronic pancreatitis; pancreatic cancer
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Special Issue Information

Dear Colleagues,

It has been known since long that natural and dietary compounds offer protection and affect the pathogenesis of chronic diseases. Especially, several dietary compounds act as chemopreventive and chemotherapeutic agents against various forms of cancer. Indeed, over the recent decades, several natural compounds have been discovered that are now widely used as anti-cancer agents, including paclitaxel, vinblastine, camptothecin, and oleuropein.

With this background, we invite submissions for papers under the title "Natural Active Substances and Cancer". This theme explores the role of bioactive compounds derived from natural sources in cancer prevention, treatment, and management. We encourage original research or reviews focusing on the mechanisms, effectiveness, and potential applications of these substances. Topics may include plant extracts, marine products, microbial metabolites, and their interactions with cancer cells, immune modulation, or synergy with conventional therapies. This is an opportunity to contribute to the growing field of natural product-based cancer research.

Prof. Dr. Yoichi Matsuo
Guest Editor

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Keywords

  • natural active substances
  • natural products and cancer
  • plant extracts
  • natural product-based cancer research
  • compounds derived from natural sources
  • chemoprevention
 

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Published Papers (1 paper)

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Research

17 pages, 1151 KiB  
Article
The Chemopreventive Effect of Ginsenoside Compound K Is Regulated by PARP-1 Hyperactivation, Which Is Promoted by p62-Dependent SIRT6 Degradation
by Sang-Hun Kim, Sung-Hwan Ki, Seok-Woo Hyeong and Seon-Hee Oh
Nutrients 2025, 17(3), 539; https://doi.org/10.3390/nu17030539 - 31 Jan 2025
Viewed by 271
Abstract
Background and aims: Ginsenoside compound K (CK), a saponin metabolite of ginseng, exerts anticancer effects; however, its molecular mechanisms of action in lung cancer remain unclear. We investigated the involvement of silent information regulator 6 (SIRT6) and poly (ADP-ribose) polymerase 1 (PARP-1) in [...] Read more.
Background and aims: Ginsenoside compound K (CK), a saponin metabolite of ginseng, exerts anticancer effects; however, its molecular mechanisms of action in lung cancer remain unclear. We investigated the involvement of silent information regulator 6 (SIRT6) and poly (ADP-ribose) polymerase 1 (PARP-1) in the anticancer effects of CK in lung cancer. Methods and Results: CK induced PARP-1 activation-mediated parthanatos via sequestosome-1/p62-mediated SIRT6 degradation and inhibited the proliferation of H460 cells. Although CK reduced procaspase-8 levels, no significant apoptotic cleavage of procaspase-3 or PARP-1 was observed. Furthermore, CK upregulated p27, p21, phospho-p53, and gamma-H2AX levels. CK increased LC3-II levels in a p62-independent manner, but p62 was upregulated by autophagy inhibition, indicating that p62 is involved in CK-induced autophagy. CK-treated cells showed typical features of parthanatos, including PARP-1 hyperactivation, intracellular redistribution of poly ADP-ribose and pro-apoptotic factors, and chromatin fragmentation. SIRT6 was degraded in a CK concentration- and time-dependent manner. SIRT6 protein was upregulated by PARP-1 inhibition, nicotinamide adenine dinucleotide (NAD)+ supplementation, antioxidants, and p62 knockdown, but was decreased by autophagy blockade. PARP-1 activation was negatively correlated with SIRT6 levels, indicating that SIRT6 and PARP-1 activation play complementary roles in CK-induced growth inhibition. Immunofluorescence staining, fractionation studies, and immunoprecipitation were used to confirm the colocalization and interaction between p62 and SIRT6. Conclusions: PARP-1 activation is promoted by p62-mediated SIRT6 degradation, which plays an important role in CK-induced growth inhibition. Therefore, SIRT6 is a potential biomarker for the chemopreventive effect of CK in lung cancer cells, but further studies on SIRT6 are needed for the clinical application of CK. Full article
(This article belongs to the Special Issue Natural Active Substances and Cancer)
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