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Effect of Natural Products on Tumors and Tumor Microenvironments

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Natural Products Chemistry".

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 4792

Special Issue Editor


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Guest Editor
Institute of Traditional Medicine and Bioscience, Daejeon Hospital of Daejeon University, Daejeon, Korea
Interests: anti-tumor drug development; anti-cancer metastasis; tumor microenvironment; natural products
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Besides conventional therapies such as surgery, radiation, and chemotherapy, molecular targeting therapy and immunotherapy have been recently showing promising results in the treatment of cancerous diseases. Despite persistent researches and impressive advances in anti-tumor therapeutics, cancer is still the leading cause of death worldwide. On the other hand, natural compounds from plants, animals, and microorganisms are attracting large attention as alternative therapeutics, adjuvant treatments, or chemopreventive agents. In particular, they often show therapeutic effects not only on tumor cells but also on the tumor microenvironment, reducing tumorigenesis, metastatic risk, and the side effects of chemo- and radiotherapy. This Special Issue aims to update our knowledge on the potential therapeutic properties of natural products against both cancer cells and their microenvironment. Studies reporting the molecular mechanisms of action of single compounds and well-characterized/standardized mixtures of natural compounds will be considered for publication.

Prof. Dr. Chang Gue Son
Guest Editor

Manuscript Submission Information

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Keywords

  • Cancer
  • Natural products
  • Bioactive compounds
  • Tumor microenvironments
  • Metastasis
  • Tumorigenesis
  • Phytochemicals

Published Papers (2 papers)

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Research

16 pages, 4122 KiB  
Article
Betulinic Acid Affects the Energy-Related Proteomic Profiling in Pancreatic Ductal Adenocarcinoma Cells
by Ching-Feng Chiu, Hsin-Yi Chang, Chun-Yine Huang, Chen-Zou Mau, Tzu-Ting Kuo, Hsiu-Chuan Lee and Shih-Yi Huang
Molecules 2021, 26(9), 2482; https://doi.org/10.3390/molecules26092482 - 24 Apr 2021
Cited by 5 | Viewed by 2201
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with a 5-year survival rate of <8%. Therefore, finding new treatment strategies against PDAC cells is an imperative issue. Betulinic acid (BA), a plant-derived natural compound, has shown great potential to combat cancer owing to [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with a 5-year survival rate of <8%. Therefore, finding new treatment strategies against PDAC cells is an imperative issue. Betulinic acid (BA), a plant-derived natural compound, has shown great potential to combat cancer owing to its versatile physiological functions. In this study, we observed the impacts of BA on the cell viability and migratory ability of PDAC cell lines, and screened differentially expressed proteins (DEPs) by an LC-MS/MS-based proteomics analysis. Our results showed that BA significantly inhibited the viability and migratory ability of PDAC cells under a relatively low dosage without affecting normal pancreatic cells. Moreover, a functional analysis revealed that BA-induced downregulation of protein clusters that participate in mitochondrial complex 1 activity and oxidative phosphorylation, which was related to decreased expressions of RNA polymerase mitochondrial (POLRMT) and translational activator of cytochrome c oxidase (TACO1), suggesting that the influence on mitochondrial function explains the effect of BA on PDAC cell growth and migration. In addition, BA also dramatically increased Apolipoprotein A1 (APOA1) expression and decreased NLR family CARD domain-containing protein 4 (NLRC4) expression, which may be involved in the dampening of PDAC migration. Notably, altered expression patterns of APOA1 and NLRC4 indicated a favorable clinical prognosis of PDAC. Based on these findings, we identified potential proteins and pathways regulated by BA from a proteomics perspective, which provides a therapeutic window for PDAC. Full article
(This article belongs to the Special Issue Effect of Natural Products on Tumors and Tumor Microenvironments)
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12 pages, 3226 KiB  
Article
Coptidis Rhizoma Extract Reverses 5-Fluorouracil Resistance in HCT116 Human Colorectal Cancer Cells via Modulation of Thymidylate Synthase
by Yong-Hwi Kang, Jin-Seok Lee, Nam-Hun Lee, Seung-Hyung Kim, Chang-Seob Seo and Chang-Gue Son
Molecules 2021, 26(7), 1856; https://doi.org/10.3390/molecules26071856 - 25 Mar 2021
Cited by 10 | Viewed by 2102
Abstract
Colorectal cancer (CRC) is a malignancy of the colon or rectum. It is ranked as the third most common cancer in both men and women worldwide. Early resection permitted by early detection is the best treatment, and chemotherapy is another main treatment, particularly [...] Read more.
Colorectal cancer (CRC) is a malignancy of the colon or rectum. It is ranked as the third most common cancer in both men and women worldwide. Early resection permitted by early detection is the best treatment, and chemotherapy is another main treatment, particularly for patients with advanced CRC. A well-known thymidylate synthase (TS) inhibitor, 5-fluorouracil (5-FU), is frequently prescribed to CRC patients; however, drug resistance is a critical limitation of its clinical application. Based on the hypothesis that Coptidis Rhizoma extract (CRE) can abolish this 5-FU resistance, we explored the efficacy and underlying mechanisms of CRE in 5-FU-resistant (HCT116/R) and parental HCT116 (HCT116/WT) cells. Compared to treatment with 5-FU alone, combination treatment with CRE and 5-FU drastically reduced the viability of HCT116/R cells. The cell cycle distribution assay showed significant induction of the G0/G1 phase arrest by co-treatment with CRE and 5-FU. In addition, the combination of CRE and 5-FU notably suppressed the activity of TS, which was overexpressed in HCT116/R cells, as compared to HCT116/WT cells. Our findings support the potential of CRE as an adjuvant agent against 5-FU-resistant colorectal cancers and indicate that the underlying mechanisms might involve inhibition of TS expression. Full article
(This article belongs to the Special Issue Effect of Natural Products on Tumors and Tumor Microenvironments)
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