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Natural Active Substances and Cancer
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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: closed (20 January 2026) | Viewed by 6318

Special Issue Editor

Prof. Dr. Yoichi Matsuo

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

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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 (4 papers)

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Research

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24 pages, 12707 KB  
Article
Malva sylvestris Flower Extract Exhibits Antineoplastic Potential Against Human Colon Cancer Cell Lines and Induces CDK2 Transcript Instability via Plant miR160-5p
by Valentina Villani and Angelo Gismondi
Nutrients 2026, 18(3), 495; https://doi.org/10.3390/nu18030495 - 2 Feb 2026
Viewed by 788
Abstract
Background: Malva sylvestris (the common mallow) is an herbaceous species widely used in ethnobotanical practices to treat gastrointestinal, hepatic and urinary inflammation. Objectives: Despite these beneficial effects on human health, the antineoplastic potential of this plant has not yet been fully explored. [...] Read more.
Background: Malva sylvestris (the common mallow) is an herbaceous species widely used in ethnobotanical practices to treat gastrointestinal, hepatic and urinary inflammation. Objectives: Despite these beneficial effects on human health, the antineoplastic potential of this plant has not yet been fully explored. Thus, in the present study, two human colon cancer cell lines (i.e., HCT-116 and Caco-2) were treated with an extract obtained from M. sylvestris flowers (MFE), whose composition in terms of phytochemicals and microRNAs has been recently published by our research group, to explore its potential bioactivity. Methods/Results: MTT and Trypan blue assays demonstrated that MFE reduced tumour cell growth without causing significant cytotoxicity or apoptosis. Following the diphenylboric acid 2-aminoethyl ester-induced fluorescence of some plant metabolites, microscopy analysis proved that MFE components crossed the cell membranes, accumulating into nuclei. Wound assay and transwell tests documented that MFE was also able to reduce cell motility and invasiveness. In both cell lines qPCR experiments demonstrated that MFE caused the over-expression of factors, like VIMENTIN and E-CADHERIN, which negatively influence epithelial–mesenchymal transition in colon cancers. However, the effects of MFE appeared to be time-, dose- and cell type-dependent. In fact, the treatment induced senescence in P53-null Caco-2 cells (i.e., ROS, β-galactosidase and P21WAF1/Cip1) and a premise of differentiation (i.e., P27Kip1) in P53-wild-type HCT-116 cells, also via the CDK2/c-MYC/AKT axis, justifying its antiproliferative property. In parallel, the transfection of tumour cells with pure synthetic miR160b-5p—a microRNA identified in M. sylvestris flowers and predicted to target the human CDK2 transcript—resulted in gene silencing, thereby suggesting its central role in mediating the cross-kingdom effects of MFE on the investigated cancer models. Conclusions: Overall, these findings open new perspectives on the common mallow as a source of potential antimetastatic compounds and on the possible use of its plant microRNAs in the development of gene therapies. Full article
(This article belongs to the Special Issue Natural Active Substances and Cancer)
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17 pages, 3264 KB  
Article
The Natural Compound CalebinA Suppresses Gemcitabine Resistance and Tumor Progression by Inhibiting Angiogenesis and Invasion Through NF-κB Signaling in Pancreatic Cancer
by Yuki Eguchi, Yoichi Matsuo, Masaki Ishida, Yuriko Uehara, Saburo Sugita, Yuki Denda, Keisuke Nonoyama, Hiromichi Murase, Tomokatsu Kato, Kenta Saito, Takafumi Sato, Hiroyuki Sagawa, Yushi Yamakawa, Ryo Ogawa, Hiroki Takahashi, Akira Mitsui and Shuji Takiguchi
Nutrients 2025, 17(16), 2641; https://doi.org/10.3390/nu17162641 - 14 Aug 2025
Viewed by 1244
Abstract
Background: Previously, we established gemcitabine (Gem)-resistant pancreatic cancer (PaCa) cell lines and showed that the acquisition of Gem resistance is accompanied by enhanced activation of the inflammatory transcription factor nuclear factor-κB (NF-κB). In this study, we focus on CalebinA, a natural compound derived [...] Read more.
Background: Previously, we established gemcitabine (Gem)-resistant pancreatic cancer (PaCa) cell lines and showed that the acquisition of Gem resistance is accompanied by enhanced activation of the inflammatory transcription factor nuclear factor-κB (NF-κB). In this study, we focus on CalebinA, a natural compound derived from the rhizomes of turmeric, known for its potent anti-inflammatory properties. It has been suggested that this compound may exert anticancer effects by downregulating the NF-κB signaling cascade. Therefore, we collaborated with Sabinsa Corporation, Japan, to explore its potential application in pancreatic cancer therapy. Methods: We used gemcitabine-resistant pancreatic cell lines to demonstrate the effect of CalebinA on cell toxicity, invasiveness, cytokine levels, NF-κB p65 activity, and tube formation in angiogenesis. Tumor volume and histopathological analysis were used to analyze the effects of CalebinA on tumors induced by the subcutaneous injection of pancreatic cell lines in mice. Results: Treatment with 10 μM CalebinA significantly inhibited NF-κB activity. Gem-resistant PaCa cells exhibited higher invasive and angiogenic capacities than non-resistant parental cells; however, these capacities were markedly suppressed by CalebinA. In vivo, intraperitoneal CalebinA administration every 3 days led to a significant reduction in tumor volume in mice bearing subcutaneous xenografts of the AsPC-1 pancreatic cancer cell line. Immunohistochemical analysis revealed that CalebinA suppressed the expression of Ki-67, CD31-positive microvessel density, and NF-κB p65. Conclusions: These findings suggest that CalebinA holds promise as a novel therapeutic agent for Gem-resistant pancreatic cancer and may be a strong candidate for clinical application. Full article
(This article belongs to the Special Issue Natural Active Substances and Cancer)
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17 pages, 2163 KB  
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
Cited by 2 | Viewed by 1832
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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Review

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24 pages, 3695 KB  
Review
Therapeutic Advances of Curcumin and Nanocurcumin in Glioblastoma: Molecular Targets, Bioavailability, and Drug Delivery
by Md Ataur Rahman, Mahesh Kumar Yadab and Meser M. Ali
Nutrients 2026, 18(2), 194; https://doi.org/10.3390/nu18020194 - 7 Jan 2026
Cited by 1 | Viewed by 1659
Abstract
Glioblastoma (GBM), the most common, invasive, and chemoresistant form of adult primary brain cancer, is characterized by rapid cell proliferation, local invasiveness, and resistance to chemotherapy (e.g., temozolomide (TMZ)) and radiation therapy. Curcumin, a bioactive polyphenol derived from Curcuma longa, has exhibited [...] Read more.
Glioblastoma (GBM), the most common, invasive, and chemoresistant form of adult primary brain cancer, is characterized by rapid cell proliferation, local invasiveness, and resistance to chemotherapy (e.g., temozolomide (TMZ)) and radiation therapy. Curcumin, a bioactive polyphenol derived from Curcuma longa, has exhibited exceptional anti-cancer properties, including anti-proliferative, pro-apoptotic, anti-inflammatory, and anti-angiogenic activities in a wide range of cancer models, including GBM. However, the clinical application of curcumin has been seriously limited by several challenges, including low water solubility, low bioavailability, rapid systemic clearance, and poor blood–brain barrier (BBB) penetration. To overcome these challenges, several nanocarrier systems to produce nanocurcumin have been developed, including liposomes, polymeric nanoparticles, solid lipid nanoparticles, dendrimers, and micelles. These nanoformulations improve the solubility, stability, systemic circulation, and target-directed delivery of curcumin to glioma cells, thereby resulting in a high level of accumulation in the glioma microenvironment. On the other hand, this work is devoted to the potential of curcumin and nanocurcumin for the treatment of GBM. The article provides a detailed review of the major molecular targets of curcumin, such as NF-κB, STAT3, PI3K/AKT/mTOR, and p53 signaling pathways, as well as recent advancements in nanotechnology-based delivery platforms that improve drug delivery across the BBB and their possible clinical translation. We also include a thorough examination of the issues, limitations, and potential opportunities associated with the clinical advancement of curcumin-based therapeutics for GBM. Full article
(This article belongs to the Special Issue Natural Active Substances and Cancer)
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