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Natural Bioactives and Phytochemicals in Cancer Prevention 2.0

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

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 11740

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Special Issue Editor

Prof. Dr. Shun-Fa Yang

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Guest Editor

Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan
Interests: cancer prevention; cancer biomarker; oral cancer; cancer metastasis; polymorphism; tumor microenvironment; matrix metalloproteinase
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Natural bioactives, or phytochemicals, generally refer to compounds exclusive to essential nutrients that have specific biological activities in humans. It is known that over 10,000 different phytochemicals possess potential preventive or supplementary effects on various diseases. Studies have shown that natural phytochemicals derived from certain plants have the capability to prevent carcinogenesis. Therefore, new active compounds responsible for the anti-cancer characteristics of dietary plants, and original active compounds exert novel function on anti-carcinogenesis, are important issues in cancer investigation. We invite the researchers to contribute original and review articles regarding the relationship between phytochemicals and cancers, including the discovery of novel anti-cancer phytochemicals and the novel signalling pathways, and signalling molecules of phytochemicals on cancer treatment.

Prof. Dr. Shun-Fa Yang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

natural bioactives
phytochemicals
cancer
metastasis
apoptosis

Related Special Issue

Natural Bioactives and Phytochemicals in Cancer Prevention in International Journal of Molecular Sciences (21 articles)

Published Papers (6 papers)

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Research

11 pages, 3133 KiB

Open AccessArticle

Dihydromyricetin Inhibited Migration and Invasion by Reducing S100A4 Expression through ERK1/2/β-Catenin Pathway in Human Cervical Cancer Cell Lines

by Min-Chieh Hsin, Yi-Hsuan Hsiao, Pei-Ni Chen, Chiao-Wen Lin, Po-Hui Wang, Shun-Fa Yang and Chung-Yuan Lee

Int. J. Mol. Sci. 2022, 23(23), 15106; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232315106 - 01 Dec 2022

Cited by 2 | Viewed by 1295

Abstract

Cervical cancer has a poor prognosis and is the fourth most common cancer among women. Dihydromyricetin (DHM), a flavonoid compound, exhibits several pharmacological activities, including anticancer effects; however, the effects of DHM on cervical cancer have received insufficient research attention. This study examined the antitumor activity and underlying mechanisms of DHM on human cervical cancer. Our results indicated that DHM inhibits migration and invasion in HeLa and SiHa cell lines. Mechanistically, RNA sequencing analysis revealed that DHM suppressed S100A4 mRNA expression in HeLa cells. Moreover, DHM inhibited the protein expressions of β-catenin and GSK3β through the regulated extracellular-signal-regulated kinase (ERK)1/2 signaling pathway. By using the ERK1/2 activator, T-BHQ, reverted β-catenin and S100A4 protein expression and cell migration, which were reduced in response to DHM. In conclusion, our study indicated that DHM inhibited cell migration by reducing the S100A4 expression through the ERK1/2/β-catenin pathway in human cervical cancer cell lines. Full article

(This article belongs to the Special Issue Natural Bioactives and Phytochemicals in Cancer Prevention 2.0)

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20 pages, 2999 KiB

Open AccessArticle

Proteomes of Residual Tumors in Curcumin-Treated Rats Reveal Changes in Microenvironment/Malignant Cell Crosstalk in a Highly Invasive Model of Mesothelioma

by Daniel L. Pouliquen, Marine Malloci, Alice Boissard, Cécile Henry and Catherine Guette

Int. J. Mol. Sci. 2022, 23(22), 13732; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232213732 - 08 Nov 2022

Cited by 1 | Viewed by 1729

Abstract

Curcumin exhibits both immunomodulatory properties and anticarcinogenic effects which have been investigated in different experimental tumor models and cancer types. Its interactions with multiple signaling pathways have been documented through proteomic studies on malignant cells in culture; however, in vivo approaches are scarce. In this study, we used a rat model of highly invasive peritoneal mesothelioma to analyze the residual tumor proteomes of curcumin-treated rats in comparison with untreated tumor-bearing rats (G1) and provide insights into the modifications in the tumor microenvironment/malignant cell crosstalk. The cross-comparing analyses of the histological sections of residual tumors from two groups of rats given curcumin twice on days 21 and 26 after the tumor challenge (G2) or four times on days 7, 9, 11 and 14 (G3), in comparison with G1, identified a common increase in caveolin-1 which linked with significant abundance changes affecting 115 other proteins. The comparison of G3 vs. G2 revealed additional features for 65 main proteins, including an increase in histidine-rich glycoprotein and highly significant abundance changes for 22 other proteins regulating the tumor microenvironment, linked with the presence of numerous activated T cells. These results highlight new features in the multiple actions of curcumin on tumor microenvironment components and cancer cell invasiveness. Full article

(This article belongs to the Special Issue Natural Bioactives and Phytochemicals in Cancer Prevention 2.0)

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19 pages, 10200 KiB

Open AccessArticle

Physapruin A Enhances DNA Damage and Inhibits DNA Repair to Suppress Oral Cancer Cell Proliferation

by Tzu-Jung Yu, Ching-Yu Yen, Yuan-Bin Cheng, Chia-Hung Yen, Jiiang-Huei Jeng, Jen-Yang Tang and Hsueh-Wei Chang

Int. J. Mol. Sci. 2022, 23(16), 8839; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23168839 - 09 Aug 2022

Cited by 8 | Viewed by 2143

Abstract

The selective antiproliferation to oral cancer cells of Physalis peruviana-derived physapruin A (PHA) is rarely reported. Either drug-induced apoptosis and DNA damage or DNA repair suppression may effectively inhibit cancer cell proliferation. This study examined the selective antiproliferation ability of PHA and explored detailed mechanisms of apoptosis, DNA damage, and repair. During an ATP assay, PHA provided high cytotoxicity to two oral cancer cell lines (CAL 27 and Ca9-22) but no cytotoxicity to two non-malignant oral cells (HGF-1 and SG). This selective antiproliferation of PHA was associated with the selective generation of reactive oxygen species (ROS) in oral cancer cells rather than in non-malignant oral cells, as detected by flow cytometry. Moreover, PHA induced other oxidative stresses in oral cancer cells, such as mitochondrial superoxide generation and mitochondrial membrane potential depletion. PHA also demonstrated selective apoptosis in oral cancer cells rather than non-malignant cells in annexin V/7-aminoactinmycin D and caspase 3/7 activity assays. In flow cytometry and immunofluorescence assays, PHA induced γH2AX expressions and increased the γH2AX foci number of DNA damages in oral cancer cells. In contrast, the mRNA expressions for DNA repair signaling, including homologous recombination (HR) and non-homologous end joining (NHEJ)-associated genes, were inhibited by PHA in oral cancer cells. Moreover, the PHA-induced changes were alleviated by the oxidative stress inhibitor N-acetylcysteine. Therefore, PHA generates selective antiproliferation, oxidative stress, and apoptosis associated with DNA damage induction and DNA repair suppression in oral cancer cells. Full article

(This article belongs to the Special Issue Natural Bioactives and Phytochemicals in Cancer Prevention 2.0)

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13 pages, 3400 KiB

Open AccessArticle

Deoxyshikonin Mediates Heme Oxygenase-1 Induction and Apoptotic Response via p38 Signaling in Tongue Cancer Cell Lines

by Chun-Yi Chuang, Chiao-Wen Lin, Chun-Wen Su, Yi-Tzu Chen, Wei-En Yang, Shun-Fa Yang and Shih-Chi Su

Int. J. Mol. Sci. 2022, 23(13), 7115; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23137115 - 26 Jun 2022

Cited by 4 | Viewed by 1690

Abstract

Deoxyshikonin (DSK), a phytochemical constituent, has been documented to elicit various oncostatic properties alone or in combination with established therapeutics. However, its role in restraining oral squamous cell carcinoma (OSCC) is mostly unclear. Here, we examined the tumor-suppressive effect of DSK and explored the molecular mechanisms underlying DSK’s activities on controlling oral cancer. Our results showed that DSK dose-dependently lessened the cell viability of tongue cancer cell lines, involving induction of cell cycle arrest at the sub-G1 phase and apoptotic cell death. Moreover, a unique signature of apoptosis-related proteins, including augmented nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) expression and caspase activation, was observed in DSK-treated tongue cancer cell lines. Furthermore, DSK-mediated upregulation of HO-1 and cleavage of caspase-9 and -3 were significantly inhibited by pharmacological blockage of p38 kinase. Collectively, these data revealed that DSK halted cell cycle progression and elicited cell apoptosis in tongue cancer cell lines, reshaping a p38-dependent profile of apoptotic proteome. Our findings provided novel insights into the therapeutic implications of a natural compound on the management of OSCC. Full article

(This article belongs to the Special Issue Natural Bioactives and Phytochemicals in Cancer Prevention 2.0)

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15 pages, 2684 KiB

Open AccessArticle

Plant Alkaloid Tetrandrine Is a Nuclear Receptor 4A1 Antagonist and Inhibits Panc-1 Cell Growth In Vitro and In Vivo

by Hyo-Seon Lee, Dae Hwan Kim, In-Seon Lee, Ji-Hyun Park, Gregory Martin, Stephen Safe, Keuk-Jun Kim, Joung-Hee Kim, Byung Ik Jang and Syng-Ook Lee

Int. J. Mol. Sci. 2022, 23(9), 5280; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23095280 - 09 May 2022

Cited by 7 | Viewed by 2290

Abstract

The orphan nuclear receptor 4A1 (NR4A1) is highly expressed in human pancreatic cancer cells and exerts pro-oncogenic activity. In a previous study, we demonstrated that fangchinoline (FCN), a natural inhibitor of nuclear NR4A1, induces NR4A1-dependent apoptosis in human pancreatic cancer cells. In this study, we evaluated FCN and its structural analogs (berbamine, isotetrandrine, tetrandrine, and tubocurarine) for their inhibitory effects on NR4A1 transactivity, and confirmed that tetrandrine (TTD) showed the highest inhibitory effect in pancreatic cancer cells. Moreover, in a tryptophan fluorescence quenching assay, TTD directly bound to the ligand binding domain (LBD) of NR4A1 with a K_D value of 10.60 μM. Treatment with TTD decreased proliferation and induced apoptosis in Panc-1 human pancreatic cancer cells in part through the reduced expression of the Sp1-dependent anti-apoptotic gene survivin and induction of ROS-mediated endoplasmic reticulum stress, which are the well-known NR4A1-dependent proapoptotic pathways. Furthermore, at a dose of 25 mg/kg/day, TTD reduced tumor growth in an athymic nude mouse xenograft model bearing Panc-1 cells. These data show that TTD is an NR4A1 antagonist and that modulation of the NR4A1-mediated pro-survival pathways is involved in the antitumor effects of TTD. Full article

(This article belongs to the Special Issue Natural Bioactives and Phytochemicals in Cancer Prevention 2.0)

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14 pages, 3982 KiB

Open AccessArticle

FLLL32 Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells by Regulating the p38 Pathway

by Chun-Wen Su, Chun-Yi Chuang, Yi-Tzu Chen, Wei-En Yang, Yi-Ping Pan, Chiao-Wen Lin and Shun-Fa Yang

Int. J. Mol. Sci. 2021, 22(21), 11860; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111860 - 01 Nov 2021

Cited by 15 | Viewed by 1868

Abstract

Oral cancer is the most common oral malignant tumor in Taiwan. Although there exist several methods for treatment, oral cancer still has a poor prognosis and high recurrence. FLLL32, a synthetic analog of curcumin with antitumor activity, is currently known to induce melanoma apoptosis and inhibit tumor growth in various cancers. However, few studies have examined the mechanisms of FLLL32 in oral cancer. In this study, we explore whether FLLL32 induces apoptosis in oral cancer. We determined that FLLL32 can inhibit the cell viability of oral cancer. Next, we analyzed the effect of FLLL32 on the cell cycle of oral cancer cells and observed that the proportion of cells in the G2/M phase was increased. Additionally, annexin-V/PI double staining revealed that FLLL32 induced apoptosis in oral cancer cells. Data from the Human Apoptosis Array revealed that FLLL32 increases the expression of cleaved caspase-3 and heme oxygenase-1 (HO-1). FLLL32 activates proteins such as caspase-8, caspase-9, caspase-3, PARP, and mitogen-activated protein kinases (MAPKs) in apoptosis-related molecular mechanisms. Moreover, by using MAPK inhibitors, we suggest that FLLL32 induces the apoptosis of oral cancer cells through the p38 MAPK signaling pathway. In conclusion, our findings suggest that FLLL32 is a potential therapeutic agent for oral cancer by inducing caspase-dependent apoptosis and HO-1 activation through the p38 pathway. We believe that the activation of HO-1 and the p38 pathway by FLLL32 represent potential targets for further research in oral cancer. Full article

(This article belongs to the Special Issue Natural Bioactives and Phytochemicals in Cancer Prevention 2.0)

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