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Mechanisms of Natural Products in the Treatment of Cancer: From Molecular Targets to Signaling Pathways

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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: closed (30 April 2022) | Viewed by 9804

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Special Issue Editors

Dr. Young-Jun Jeon

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Guest Editor

Department of Integrative Biotechnology, Sungkyunkwan University, Seobu-ro, Jangan-gu, Suwon-si, Gyeong gi-do 16419, Korea
Interests: cancer cell biology; drug resistance; liquid biopsy; circulating tumor nucleic acids; next generation sequencing; bioinformatics; noncoding RNA

Dr. Jong Kook Park

E-Mail Website
Guest Editor

Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 24252, Republic of Korea
Interests: miRNA; non-coding RNA; gene expression analysis; biomarkers; cancer microenvironment; drug resistance; cancer therapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Natural products originating from various resources, such as plants, microorganisms, and other living organisms, have been investigated for their therapeutic potential against cancer and are the basis of many of the anti-cancer drugs currently applied in clinical use. Accumulating evidence has showed that natural products modulate the tumor microenvironment and regulate diverse cellular signaling pathways by modulating the activity or expression, or both, of their molecular targets, such as proteins and noncoding RNAs (microRNAs, long noncoding RNAs, and circular RNAs), thus consequently affecting apoptotic cell death, cell proliferation, migration/invasion, angiogenesis, metastasis, and so forth. Considerable progress has also been made in evaluating the combined effect of natural products with other types of cancer treatment to subdue therapeutic resistance. Nonetheless, a better understanding of the mode of action of natural products is necessary to develop more successful therapeutic strategies against cancer.

The aim of this Special Issue on “Mechanisms of Natural Products in the Treatment of Cancer: From Molecular Targets to Signaling Pathways” is to raise our understanding of the feature of natural products, ultimately for the development of a novel approach for cancer treatment. This Special Issue warmly welcomes original research articles and review articles addressing the recent advances and emerging trends in the field of natural products. Topics include, but are not limited to:

Novel natural products eliciting anti-cancer activity;
Targets (proteins and noncoding RNAs) of natural products;
Effects of natural products on microenvironment and cellular signaling pathways;
Natural products in combination with other cancer therapies

Dr. Young-Jun Jeon
Dr. Jong Kook Park
Guest Editors

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.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

cancer
natural product
target identification
noncoding RNA
microenvironment
proliferation
migration/invasion
metastasis
cellular signaling pathways
drug combinatio

Published Papers (4 papers)

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Research

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15 pages, 2336 KiB

Open AccessArticle

SK119, a Novel Shikonin Derivative, Leads to Apoptosis in Melanoma Cell Lines and Exhibits Synergistic Effects with Vemurafenib and Cobimetinib

by Nadine Kretschmer, Christin Durchschein, Antje Hufner, Beate Rinner, Birgit Lohberger and Rudolf Bauer

Int. J. Mol. Sci. 2022, 23(10), 5684; https://doi.org/10.3390/ijms23105684 - 19 May 2022

Cited by 1 | Viewed by 1781

Abstract

Melanoma is a complex and heterogenous disease, displays the deadliest form of skin cancer, and accounts for approx. 80% of all skin cancer deaths. In this study, we reported on the synthesis and pharmacological effects of a novel shikonin derivative (SK119), which is active in a nano-molar range and exhibits several promising in vitro effects in different human melanoma cells. SK119 was synthesized from shikonin as part of our search for novel, promising shikonin derivatives. It was screened against a panel of melanoma and non-tumorigenic cell lines using XTT viability assays. Moreover, we studied its pharmacological effects using apoptosis and Western blot experiments. Finally, it was combined with current clinically used melanoma therapeutics. SK119 exhibited IC₅₀ values in a nano-molar range, induced apoptosis and led to a dose-dependent increase in the expression and protein phosphorylation of HSP27 and HSP90 in WM9 and MUG-Mel 2 cells. Combinatorial treatment, which is highly recommended in melanoma, revealed the synergistic effects of SK119 with vemurafenib and cobimetinib. SK119 treatment changed the expression levels of apoptosis genes and death receptor expression and exhibited synergistic effects with vemurafenib and cobimetinib in human melanoma cells. Further research indicates a promising potential in melanoma therapy. Full article

(This article belongs to the Special Issue Mechanisms of Natural Products in the Treatment of Cancer: From Molecular Targets to Signaling Pathways)

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14 pages, 1589 KiB

Open AccessArticle

Opposing Effects of Chelidonine on Tyrosine and Serine Phosphorylation of STAT3 in Human Uveal Melanoma Cells

by István Csomós, Péter Nagy, Csenge Filep, István Rebenku, Enikő Nizsalóczki, Tamás Kovács, György Vámosi, László Mátyus and Andrea Bodnár

Int. J. Mol. Sci. 2021, 22(23), 12974; https://doi.org/10.3390/ijms222312974 - 30 Nov 2021

Cited by 4 | Viewed by 1872

Abstract

STAT3 is a transcription factor that regulates various cellular processes with oncogenic potential, thereby promoting tumorigenesis when activated uncontrolled. STAT3 activation is mediated by its tyrosine phosphorylation, triggering dimerization and nuclear translocation. STAT3 also contains a serine phosphorylation site, with a postulated regulatory role in STAT3 activation and G2/M transition. Interleukin-6, a major activator of STAT3, is present in elevated concentrations in uveal melanomas, suggesting contribution of dysregulated STAT3 activation to their pathogenesis. Here, we studied the impact of chelidonine on STAT3 signaling in human uveal melanoma cells. Chelidonine, an alkaloid isolated from Chelidonium majus, disrupts microtubules, causes mitotic arrest and provokes cell death in numerous tumor cells. According to our flow cytometry and confocal microscopy data, chelidonine abrogated IL-6-induced activation and nuclear translocation, but amplified constitutive serine phosphorylation of STAT3. Both effects were restricted to a fraction of cells only, in an all-or-none fashion. A partial overlap could be observed between the affected subpopulations; however, no direct connection could be proven. This study is the first proof on a cell-by-cell basis for the opposing effects of a microtubule-targeting agent on the two types of STAT3 phosphorylation. Full article

(This article belongs to the Special Issue Mechanisms of Natural Products in the Treatment of Cancer: From Molecular Targets to Signaling Pathways)

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14 pages, 3364 KiB

Open AccessArticle

Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer

by Cristina Minnelli, Laura Cianfruglia, Emiliano Laudadio, Giovanna Mobbili, Roberta Galeazzi and Tatiana Armeni

Int. J. Mol. Sci. 2021, 22(21), 11833; https://doi.org/10.3390/ijms222111833 - 31 Oct 2021

Cited by 29 | Viewed by 2217

Abstract

The epidermal growth factor receptor (EGFR) is one of the most well-studied molecular targets in non-small cell lung cancer (NSCLC) and tyrosine kinase inhibitors have been shown to be effective in the treatment of advanced NSCLC. Nevertheless, the efficacy of tyrosine kinase inhibitors could be compromised by additional mutations in EGFR and compensatory activations of other pathways. Epigallocatechin-3-gallate (EGCG), the main bioactive molecule in green tea, acts as a tyrosine kinase inhibitor toward cancer cells overexpressing EGFR (wild-type). However, little information has been reported on the effect of EGCG on EGFR with activating mutations. In this study, we evaluated the ability of EGCG to inhibit EGFR signaling activation in three different NSCLC cell lines containing wild-type EGFR or EGFR with additional mutations. The effect on proliferation, apoptosis, migration, and vinculin expression was then studied. Overall, our results demonstrate that EGCG polyphenol inhibits cell proliferation and migration in NSCLC cell lines, although with different efficacy and mechanisms. These data may be of interest for an evaluation of the use of EGCG as an adjunct to NSCLC therapies. Full article

(This article belongs to the Special Issue Mechanisms of Natural Products in the Treatment of Cancer: From Molecular Targets to Signaling Pathways)

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Review

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15 pages, 895 KiB

Open AccessReview

Mechanisms of Natural Extracts of Andrographis paniculata That Target Lipid-Dependent Cancer Pathways: A View from the Signaling Pathway

by Ruth Naomi, Hasnah Bahari, Zhi Yi Ong, Yong Yoke Keong, Hashim Embong, Retnagowri Rajandram, Soo Huat Teoh, Fezah Othman, Rosnani Hasham, Khoo Boon Yin, Priyatharisni Kaniappan, Muhammad Dain Yazid and Zainul Amiruddin Zakaria

Int. J. Mol. Sci. 2022, 23(11), 5972; https://doi.org/10.3390/ijms23115972 - 26 May 2022

Cited by 6 | Viewed by 3271

Abstract

Andrographis paniculata is a local medicinal plant that is widely cultivated in Malaysia. It is comprised of numerous bioactive compounds that can be isolated using water, ethanol or methanol. Among these compounds, andrographolide has been found to be the major compound and it exhibits varieties of pharmacological activities, including anti-cancer properties, particularly in the lipid-dependent cancer pathway. Lipids act as crucial membrane-building elements, fuel for energy-demanding activities, signaling molecules, and regulators of several cellular functions. Studies have shown that alterations in lipid composition assist cancer cells in changing microenvironments. Thus, compounds that target the lipid pathway might serve as potential anti-cancer therapeutic agents. The purpose of this review is to provide an overview of the medicinal chemistry and pharmacology of A. paniculata and its active compounds in terms of anti-cancer activity, primary mechanism of action, and cellular targets, particularly in the lipid-dependent cancer pathway. Full article

(This article belongs to the Special Issue Mechanisms of Natural Products in the Treatment of Cancer: From Molecular Targets to Signaling Pathways)

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