Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.3
2.4
Journals
Medicina
Special Issues
Natural Products for Cancer Treatment: From Traditional Medicine to Modern...
share announcement

Natural Products for Cancer Treatment: From Traditional Medicine to Modern Drug Discovery

A special issue of Medicina (ISSN 1648-9144).

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 20972

Special Issue Editor

Dr. Jincheng Wang

E-Mail Website
Guest Editor
Faculty of Medicine, Hokkaido University, Sapporo 060-8638, Japan
Interests: natural products; machine learning; image biomarker; cancer treatment; prediction model

Special Issue Information

Dear Colleagues,

Natural products, including their primary and secondary metabolites, are small molecules and complex structures derived from any organism. Over the past decades, natural products have enlightened the advent of modern medical science, and natural product-based modern drug discovery has contributed to one of the most remarkable achievements in pharmaceutical science. Cancer has been highlighted as one of the leading causes of death globally. Conventional cancer therapies, including surgery, radiation, and chemotherapy, could lead to cancer recurrence, the emergence of resistance, and the development of severe side effects. Currently, the limited efficacy and increased toxicity caused by conventional anticancer therapies have encouraged scientists to focus on discovering and developing new anticancer agents derived from traditional natural products. Most of the anticancer drugs that have shown high efficiency in clinical use are obtained from plants, aquatic organisms, and microorganisms. The anticancer effect of these natural products is mediated by different mechanisms, including apoptosis induction, immune system modulation, and angiogenesis inhibition. These application cases highlight the role of natural products in modern drug discovery for cancer treatment. Importantly, some rapidly developing technologies, such as informatics and computational technology, have provided a systematic and efficient tool to investigate natural products and thus extend drug discovery.

Topics of interest include but are not limited to the following:

  1. Informatics and computational methods to discover novel drugs based on natural products.
  2. Informatics and computational methods to identify drug–disease interaction targets.
  3. Clinical studies investigating the effect of natural products in cancer treatment.
  4. Clinical validation of natural products as adjuvant therapy in cancer treatment strategies.
  5. Network pharmacology analysis for the detection of potential cancer treatment strategies.
  6. Digital online database recording putative or validated natural product targets.
  7. Software tools or online web servers to assist natural product-based drug discovery.
  8. Review articles summarizing the recent technological developments in natural product-based drug discovery, especially for cancers.

Dr. Jincheng Wang
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.

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. Medicina is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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 treatment
  • natural products
  • network pharmacology analysis
  • clinical validation
  • drug discovery
  • bioinformatics
  • drug target mining
  • machine learning
  • drug–disease interaction targets

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (6 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

14 pages, 2551 KiB  
Article
Exploring the Apoptotic-Induced Biochemical Mechanism of Traditional Thai Herb (Kerra™) Extract in HCT116 Cells Using a Label-Free Proteomics Approach
by Jeeraprapa Siriwaseree, Yodying Yingchutrakul, Pawitrabhorn Samutrtai, Chanat Aonbangkhen, Pussadee Srathong, Sucheewin Krobthong and Kiattawee Choowongkomon
Medicina 2023, 59(8), 1376; https://doi.org/10.3390/medicina59081376 - 27 Jul 2023
Cited by 2 | Viewed by 4881
Abstract
Background and Objectives: Natural products have proven to be a valuable source for the discovery of new candidate drugs for cancer treatment. This study aims to investigate the potential therapeutic effects of “Kerra™”, a natural extract derived from a mixture of nine medicinal [...] Read more.
Background and Objectives: Natural products have proven to be a valuable source for the discovery of new candidate drugs for cancer treatment. This study aims to investigate the potential therapeutic effects of “Kerra™”, a natural extract derived from a mixture of nine medicinal plants mentioned in the ancient Thai scripture named the Takxila Scripture, on HCT116 cells. Materials and Methods: In this study, the effect of the Kerra™ extract on cancer cells was assessed through cell viability assays. Apoptotic activity was evaluated by examining the apoptosis characteristic features. A proteomics analysis was conducted to identify proteins and pathways associated with the extract’s mechanism of action. The expression levels of apoptotic protein markers were measured to validate the extract’s efficacy. Results: The Kerra™ extract demonstrated a dose-dependent inhibitory effect on the cells, with higher concentrations leading to decreased cell viability. Treatment with the extract for 72 h induced characteristic features of early and late apoptosis, as well as cell death. An LC-MS/MS analysis identified a total of 3406 proteins. The pathway analysis revealed that the Kerra™ extract stimulated apoptosis and cell death in colorectal cancer cell lines and suppressed cell proliferation in adenocarcinoma cell lines through the EIF2 signaling pathway. Upstream regulatory proteins, including cyclin-dependent kinase inhibitor 1A (CDKN1A) and MYC proto-oncogene, bHLH transcription factor (MYC), were identified. The expressions of caspase-8 and caspase-9 were significantly elevated by the Kerra™ extract compared to the chemotherapy drug Doxorubicin (Dox). Conclusions: These findings provide strong evidence for the ability of the Kerra™ extract to induce apoptosis in HCT116 colon cancer cells. The extract’s efficacy was demonstrated by its dose-dependent inhibitory effect, induction of apoptotic activity, and modulation of key proteins involved in cell death and proliferation pathways. This study highlights the potential of Kerra™ as a promising therapeutic agent in cancer treatment. Full article
(This article belongs to the Special Issue Natural Products for Cancer Treatment: From Traditional Medicine to Modern Drug Discovery)
►▼ Show Figures

Figure 1

13 pages, 9225 KiB  
Article
Comprehensive Investigation Illustrates the Role of M2 Macrophages and Its Related Genes in Pancreatic Cancer
by Danying Zhang, Wenqing Tang, Xizhong Shen, Shuqiang Weng and Ling Dong
Medicina 2023, 59(4), 717; https://doi.org/10.3390/medicina59040717 - 6 Apr 2023
Cited by 2 | Viewed by 3056
Abstract
Background and Objectives: M2 macrophages play an important role in cancers. Our study aimed to illustrate the effect of M2 macrophages in pancreatic cancer (PC). Materials and Methods: The open-access data used for analysis were downloaded from The Cancer Genome Atlas Program database, as [...] Read more.
Background and Objectives: M2 macrophages play an important role in cancers. Our study aimed to illustrate the effect of M2 macrophages in pancreatic cancer (PC). Materials and Methods: The open-access data used for analysis were downloaded from The Cancer Genome Atlas Program database, as well as some online databases. R software was mainly used for data analysis based on the specific packages. Results: Here, we comprehensively investigated the role of M2 macrophages and their related genes in PC. We performed the biological enrichment of M2 macrophages in PC. Meanwhile, we identified adenosine A3 receptor (TMIGD3) as the interest gene for further analysis. The single-cell analysis showed that was mainly expressed in the Mono/Macro cells based on the data from multiple data cohorts. Biological investigation showed that TMIGD3 was primarily enriched in angiogenesis, pancreas-beta cells and TGF-beta signaling. Tumor microenvironment analysis indicated that TMIGD3 was positively correlated with monocyte_MCPCOUNTER, NK cell_MCPCOUNTER, macrophages M2_CIBERSORT, macrophage_EPIC, neutrophil_TIMER and endothelial cell_MCPCOUNTER. Interestingly, we determined that all the immune functions quantified by single sample gene set enrichment analysis algorithms were activated in the patients with high TMIGD3 expression. Conclusions: Our results provide a novel direction for the research focused on the M2 macrophages in PC. Meanwhile, TMIGD3 was identified as an M2 macrophage-related biomarker for PC. Full article
(This article belongs to the Special Issue Natural Products for Cancer Treatment: From Traditional Medicine to Modern Drug Discovery)
►▼ Show Figures

Figure 1

12 pages, 3269 KiB  
Article
Screening and Bioinformatics Analyses of Key miRNAs Associated with Toll-like Receptor Activation in Gastric Cancer Cells
by Xiong Huang, Zhen Ma and Wei Qin
Medicina 2023, 59(3), 511; https://doi.org/10.3390/medicina59030511 - 6 Mar 2023
Cited by 4 | Viewed by 2864
Abstract
Background and Objectives: To screen key miRNAs and their target genes related to Toll-like receptor (TLR) activation in gastric cancer (GC) cells and analyze them bioinformatically. Materials and Methods: Venn diagrams were obtained to screen miRNAs that were upregulated/downregulated in both [...] Read more.
Background and Objectives: To screen key miRNAs and their target genes related to Toll-like receptor (TLR) activation in gastric cancer (GC) cells and analyze them bioinformatically. Materials and Methods: Venn diagrams were obtained to screen miRNAs that were upregulated/downregulated in both GSE54129 and GSE164174. The miRTarBase database was used to predict the target genes of upregulated miRNAs. The differentially expressed genes in the regulatory network were analyzed. miR-16-5p expression in different tissue samples and the variations in the methylation states of four hub genes were measured. Results: We found that GSE54129 included 21 normal gastric tissues and 111 gastric cancer tissues, GSE164174 included 1417 normal gastric tissues and 1423 gastric cancer tissues. Venn diagram analysis results showed that compared with the control group, a total of 68 DEmiRNAs were upregulated in the GSE54129 and GSE164174 datasets, and no common downregulated DEmiRNAs were found. On further analysis of the GSE108345 dataset, we obtained the competing endogenous RNA (ceRNA) network associated with the activation of TLRs, and listed the top 10 lncRNA–miRNA–mRNA networks, including 10 miRNAs, 86 mRNA and 134 lncRNAs. Cytological HuBBA scores yielded a total of 1 miRNA, 16 mRNAs and 45 lncRNAs, of which miR-16-5p scored the highest as it was considered a key miRNA for TLR activation in GC cells, which are important in response against microorganisms. The results of Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that endocytosis, microRNAs in cancer and the PI3K-Akt signaling pathway are related to TLR signaling. The results of in vivo experiments indicated that miR-16-5p was highly expressed in gastric cancer cells and tissues. Conclusions: Hsa-miR-16-5p’s target genes mainly play a role by regulating the expression of four genes—MCL1, AP2B1, LAMB1, and RAB11FIP2. The findings provide a scientific basis for the development of immunotherapy for GC. Full article
(This article belongs to the Special Issue Natural Products for Cancer Treatment: From Traditional Medicine to Modern Drug Discovery)
►▼ Show Figures

Figure 1

16 pages, 4910 KiB  
Article
Identification of a Novel Gene Signature Based on Kinesin Family Members to Predict Prognosis in Glioma
by Dongxiao Pan, Xixi Fang and Jiping Li
Medicina 2023, 59(2), 414; https://doi.org/10.3390/medicina59020414 - 20 Feb 2023
Cited by 2 | Viewed by 2713
Abstract
Background and Objectives: Extensive research indicates that the kinesin superfamily (KIFs) regulates tumor progression. Nonetheless, the potential prognostic and therapeutic role of KIFs in glioma has been limited. Materials and Methods: Four independent cohorts from The Cancer Genome Atlas (TCGA) database and the [...] Read more.
Background and Objectives: Extensive research indicates that the kinesin superfamily (KIFs) regulates tumor progression. Nonetheless, the potential prognostic and therapeutic role of KIFs in glioma has been limited. Materials and Methods: Four independent cohorts from The Cancer Genome Atlas (TCGA) database and the Chinese Glioma Genome Atlas (CGGA) database were generated into a large combination cohort for identification of the prognostic signature. Following that, systematic analyses of multi-omics data were performed to determine the differences between the two groups. In addition, IDH1 was selected for the differential expression analysis. Results: The signature consists of five KIFs (KIF4A, KIF26A, KIF1A, KIF13A, and KIF13B) that were successfully identified. Receiver operating characteristic (ROC) curves indicated the signature had a suitable performance in prognosis prediction with the promising predictive area under the ROC curve (AUC) values. We then explored the genomic features differences, including immune features and tumor mutation status between high- and low-risk groups, from which we found that patients in the high-risk group had a higher level of immune checkpoint modules, and IDH1 was identified mutated more frequently in the low-risk group. Results of gene set enrichment analysis (GSEA) analysis showed that the E2F target, mitotic spindle, EMT, G2M checkpoint, and TNFa signaling were significantly activated in high-risk patients, partially explaining the differential prognosis between the two groups. Moreover, we also verified the five signature genes in the Human Protein Atlas (HPA) database. Conclusion: According to this study, we were able to classify glioma patients based on KIFs in a novel way. More importantly, the discovered KIFs-based signature and related characteristics may serve as a candidate for stratification indicators in the future for gliomas. Full article
(This article belongs to the Special Issue Natural Products for Cancer Treatment: From Traditional Medicine to Modern Drug Discovery)
►▼ Show Figures

Figure 1

16 pages, 6074 KiB  
Article
LINC00941 Promotes Cell Malignant Behavior and Is One of Five Costimulatory Molecule-Related lncRNAs That Predict Prognosis in Renal Clear Cell Carcinoma
by Huafeng Pan, Wei Wei, Guanghou Fu, Jiaren Pan and Baiye Jin
Medicina 2023, 59(2), 187; https://doi.org/10.3390/medicina59020187 - 17 Jan 2023
Cited by 4 | Viewed by 2516
Abstract
Background and Objectives: A significant role was played by costimulatory molecules in renal cancer. However, the lncRNAs regulating costimulatory molecules have not been fully investigated. Materials and Methods: Data from the next-sequence file and clinical data were downloaded from the Cancer Genome [...] Read more.
Background and Objectives: A significant role was played by costimulatory molecules in renal cancer. However, the lncRNAs regulating costimulatory molecules have not been fully investigated. Materials and Methods: Data from the next-sequence file and clinical data were downloaded from the Cancer Genome Atlas (TCGA) database. All analyses were conducted using the R and GraphPad Prism software. Results: A total of 1736 costimulatory molecule-related lncRNAs were determined under the threshold of |Cor| > 0.5 and p-value < 0.001. Furthermore, a prognosis prediction signature consisting of five lncRNAs: LINC00941, AC016773.1, AL162171.1, HOTAIRM1, and AL109741.1 was established with great prediction ability. By combining risk score and clinical parameters, a nomogram plot was constructed for better clinical practice. A biological enrichment analysis indicated that E2F targets, coagulation, IL6/JAK/STAT3 signaling, G2/M checkpoint, and allograft rejection pathways were activated in high-risk patients. Furthermore, a higher infiltration level of resting CD4+ T cell, M2 macrophage, and resting mast cells, while a lower CD8+ T cell infiltration was observed in high-risk patients. It is worthy of note that, low-risk patients might respond better to PD-1 checkpoint therapy. A correlation analysis of LINC00941 revealed that it was positively correlated with Th2 cells, Th1 cells, macrophages, and Treg cells, but negatively correlated with Th17 cells. A pathway enrichment analysis indicated that the pathways of the inflammatory response, G2M checkpoint, and IL6/JAK/STAT3 signaling were significantly activated in patients with high LINC00941 expression. In vitro experiments indicated that LINC00941 can enhance the malignant biological behaviors of renal cancer cells. Conclusions: Our study established a costimulatory molecule-related lncRNAs-based prognosis model with a great prediction prognosis. In addition, LINC00941 could enhance the malignant biological behaviors of renal cancer cells. Full article
(This article belongs to the Special Issue Natural Products for Cancer Treatment: From Traditional Medicine to Modern Drug Discovery)
►▼ Show Figures

Figure 1

20 pages, 4572 KiB  
Article
ARHGAP21 Is Involved in the Carcinogenic Mechanism of Cholangiocarcinoma: A Study Based on Bioinformatic Analyses and Experimental Validation
by Zhihuai Wang, Siyuan Wu, Gaochao Wang, Zhen Yang, Yinjie Zhang, Chunfu Zhu and Xihu Qin
Medicina 2023, 59(1), 139; https://doi.org/10.3390/medicina59010139 - 10 Jan 2023
Cited by 2 | Viewed by 2883
Abstract
Background and Objectives: Rho GTPase-activating protein (RhoGAP) is a negative regulatory element of Rho GTPases and participates in tumorigenesis. Rho GTPase-activating protein 21 (ARHGAP21) is one of the RhoGAPs and its role in cholangiocarcinoma (CCA) has never been disclosed in any publications. Materials [...] Read more.
Background and Objectives: Rho GTPase-activating protein (RhoGAP) is a negative regulatory element of Rho GTPases and participates in tumorigenesis. Rho GTPase-activating protein 21 (ARHGAP21) is one of the RhoGAPs and its role in cholangiocarcinoma (CCA) has never been disclosed in any publications. Materials and Methods: The bioinformatics public datasets were utilized to investigate the expression patterns and mutations of ARHGAP21 as well as its prognostic significance in CCA. The biological functions of ARHGAP21 in CCA cells (RBE and Hccc9810 cell) were evaluated by scratch assay, cell counting kit-8 assay (CCK8) assay, and transwell migration assay. In addition, the underlying mechanism of ARHGAP21 involved in CCA was investigated by the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and the most significant signaling pathway was identified through gene set enrichment analysis (GSEA) and the Western blot method. The ssGSEA algorithm was further used to explore the immune-related mechanism of ARHGAP21 in CCA. Results: The ARHGAP21 expression in CCA tissue was higher than it was in normal tissue, and missense mutation was the main alteration of ARHGAP21 in CCA. Moreover, the expression of ARHGAP21 had obvious differences in patients with different clinical characteristics and it had great prognostic significance. Based on cell experiments, we further observed that the proliferation ability and migration ability of the ARHGAP21-knockdown group was reduced in CCA cells. Several pathological signaling pathways correlated with proliferation and migration were determined by GO and KEGG analysis. Furthermore, the PI3K/Akt signaling pathway was the most significant one. GSEA analysis further verified that ARHGAP21 was highly enriched in PI3K/Akt signaling pathway, and the results of Western blot suggested that the phosphorylated PI3K and Akt were decreased in the ARHGAP21-knockdown group. The drug susceptibility of the PI3K/Akt signaling pathway targeted drugs were positively correlated with ARHGAP21 expression. Moreover, we also discovered that ARHGAP21 was correlated with neutrophil, pDC, and mast cell infiltration as well as immune-related genes in CCA. Conclusions: ARHGAP21 could promote the proliferation and migration of CCA cells by activating the PI3K/Akt signaling pathway, and ARHGAP21 may participate in the immune modulating function of the tumor microenvironment. Full article
(This article belongs to the Special Issue Natural Products for Cancer Treatment: From Traditional Medicine to Modern Drug Discovery)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop