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Feature Papers in Cancer Biology and Anticancer Therapeutics
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Feature Papers in Cancer Biology and Anticancer Therapeutics

A special issue of Medicines (ISSN 2305-6320). This special issue belongs to the section "Cancer Biology and Anticancer Therapeutics".

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 22782

Special Issue Editor

Prof. Dr. Seiichi Tanuma

E-Mail Website
Guest Editor
1. Department of Genomic Medicinal Science, Research Institute for Science and Technology, Organization for Research Advancement, Tokyo University of Science, Noda, Chiba 278-8510, Japan
2. Department of Biochemistry, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Chiba 278-8510, Japan
Interests: apoptosis; NAD+ metabolism; poly(ADP-ribosyl)ation; post-translational modification; DNA replication; DNA repair; carcinogenesis; Warburg effect; neuro-inflammation; neuronal disorders; aging; transcription regulation; in silico drug design; AI medicine; anti-cancer drug; anti-inflammatory drug

Special Issue Information

Dear colleagues,

We are pleased to announce the Special Issue entitled “Feature Papers in Cancer Biology and Anticancer Therapeutics”. This Special Issue aims to discuss new knowledge and share innovative ideas in the anticancer research field.

Cancer is a complex disease involving genetic/epigenetic alterations and multiple pathogenetic mechanisms. Investigation of the differential characteristics of various types of cancer cells, which distinguish them from normal cells, allows for the identification of cancer-specific targets. The principle of cancer chemo- and immune-therapies is based on the molecular targeting of the vulnerabilities of cancer cells inducing cell death by apoptosis.

In this Special Issue, we focus attention on novel target-based anticancer agents and therapeutics that exploit the vulnerabilities of cancer cells. We welcome the submission of research and review articles on the development of new anticancer agents and therapeutics.

Prof. Dr. Seiichi Tanuma
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. Medicines is an international peer-reviewed open access quarterly 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 1400 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

  • anticancer drugs
  • cancer metabolism
  • cancer inflammatory microenvironment
  • cancer biomarkers
  • cancer therapy

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

Published Papers (5 papers)

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Research

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11 pages, 1994 KiB  
Article
A Combination of GM-CSF and Released Factors from Gamma-Irradiated Tumor Cells Enhances the Differentiation of Macrophages from Bone Marrow Cells and Their Antigen-Presenting Function and Polarization to Type 1
by Lichao Chen, Shoji Imamichi, Ying Tong, Yuka Sasaki, Takae Onodera, Satoshi Nakamura, Hiroshi Igaki, Jun Itami and Mitsuko Masutani
Medicines 2021, 8(7), 35; https://doi.org/10.3390/medicines8070035 - 4 Jul 2021
Cited by 1 | Viewed by 4211
Abstract
Granulocyte-macrophage colony-stimulating factor (GM-CSF) promotes dendritic cell differentiation from precursors, and consequently, enhances the antigen presentation process and adaptive immune responses. With such functions, GM-CSF has been used as immunotherapy in combination with radiotherapy for cancer treatment to augment the survival and activity [...] Read more.
Granulocyte-macrophage colony-stimulating factor (GM-CSF) promotes dendritic cell differentiation from precursors, and consequently, enhances the antigen presentation process and adaptive immune responses. With such functions, GM-CSF has been used as immunotherapy in combination with radiotherapy for cancer treatment to augment the survival and activity of immune cells. However, an immune-suppressive tumor microenvironment may cause anergy of T cells. It has also been reported that GM-CSF contributes to the development of myeloid-derived suppressor cells from the precursors. In this study, to analyze the combined effect of GM-CSF and released factors from cancer cells after gamma-ray irradiation on bone marrow cell differentiation and dynamics, we established an in vitro culture system using mouse bone marrow cells, GM-CSF, and conditioned medium from gamma ray irradiated mouse melanoma B16 cells at 24 Gy. We analyzed the gene expression changes of the bone marrow-derived cells on day 6. The results showed that GM-CSF dose-dependently enhanced the differentiation of macrophages from bone marrow cells, their antigen-presenting function and polarization to type I. The results implied the induced macrophages from the bone marrow may potentially contribute to tumor immune responses in a systemic manner when GM-CSF is boosted during photon-beam radiation therapy. Full article
(This article belongs to the Special Issue Feature Papers in Cancer Biology and Anticancer Therapeutics)
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11 pages, 3294 KiB  
Article
β-Thujaplicin Enhances TRAIL-Induced Apoptosis via the Dual Effects of XIAP Inhibition and Degradation in NCI-H460 Human Lung Cancer Cells
by Saki Seno, Minori Kimura, Yuki Yashiro, Ryutaro Kimura, Kanae Adachi, Aoi Terabayashi, Mio Takahashi, Takahiro Oyama, Hideaki Abe, Takehiko Abe, Sei-ichi Tanuma and Ryoko Takasawa
Medicines 2021, 8(6), 26; https://doi.org/10.3390/medicines8060026 - 2 Jun 2021
Cited by 4 | Viewed by 4634
Abstract
Background: β-thujaplicin, a natural tropolone derivative, has anticancer effects on various cancer cells via apoptosis. However, the apoptosis regulatory proteins involved in this process have yet to be revealed. Methods: Trypan blue staining, a WST-8 assay, and a caspase-3/7 activity assay were [...] Read more.
Background: β-thujaplicin, a natural tropolone derivative, has anticancer effects on various cancer cells via apoptosis. However, the apoptosis regulatory proteins involved in this process have yet to be revealed. Methods: Trypan blue staining, a WST-8 assay, and a caspase-3/7 activity assay were used to investigate whether β-thujaplicin sensitizes cancer cells to TNF-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis. Additionally, western blotting was performed to clarify the effects of β-thujaplicin on X-linked inhibitor of apoptosis protein (XIAP) in NCI-H460 cells and a fluorescence polarization binding assay was used to evaluate the binding-inhibitory activity of β-thujaplicin against XIAP-BIR3. Results: β- and γ-thujaplicins decreased the viability of NCI-H460 cells in a dose-dependent manner; they also sensitized the cells to TRAIL-induced cell growth inhibition and apoptosis. β-thujaplicin significantly potentiated the apoptosis induction effect of TRAIL on NCI-H460 cells, which was accompanied by enhanced caspase-3/7 activity. Interestingly, β-thujaplicin treatment in NCI-H460 cells decreased XIAP levels. Furthermore, β-thujaplicin was able to bind XIAP-BIR3 at the Smac binding site. Conclusions: These findings indicate that β-thujaplicin could enhance TRAIL-induced apoptosis in NCI-H460 cells via XIAP inhibition and degradation. Thus, the tropolone scaffold may be useful for designing novel nonpeptidic small-molecule inhibitors of XIAP and developing new types of anticancer drugs. Full article
(This article belongs to the Special Issue Feature Papers in Cancer Biology and Anticancer Therapeutics)
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12 pages, 2365 KiB  
Article
Discovery of Novel eEF2K Inhibitors Using HTS Fingerprint Generated from Predicted Profiling of Compound-Protein Interactions
by Atsushi Yoshimori, Enzo Kawasaki, Ryuta Murakami and Chisato Kanai
Medicines 2021, 8(5), 23; https://doi.org/10.3390/medicines8050023 - 20 May 2021
Cited by 1 | Viewed by 4266
Abstract
Background: Eukaryotic elongation factor 2 kinase (eEF2K) regulates the elongation stage of protein synthesis by phosphorylating eEF2, a process related to various diseases including cancer and cardiovascular and neurodegenerative diseases. In this study, we describe the identification of novel eEF2K inhibitors using high-throughput [...] Read more.
Background: Eukaryotic elongation factor 2 kinase (eEF2K) regulates the elongation stage of protein synthesis by phosphorylating eEF2, a process related to various diseases including cancer and cardiovascular and neurodegenerative diseases. In this study, we describe the identification of novel eEF2K inhibitors using high-throughput screening fingerprints (HTSFP) generated from predicted profiling of compound-protein interactions (CPIs). Methods: We utilized computationally generated HTSFPs referred to as chemical genomics-based fingerprint (CGBFP). Generally, HTSFPs are generated from multiple biochemical or cell-based assay data. On the other hand, CGBFPs are generated from computational prediction of CPIs using the Chemical Genomics-Based Virtual Screening (CGBVS) method. Therefore, CGBFPs do not have missing information mainly caused by the absence of assay data. Results: Chemogenomics-Based Similarity Profiling (CGBSP) of the screening library (2.6 million compounds) yielded 27 compounds which were evaluated for in vitro eEF2K inhibitory activity. Three compounds with interesting results were identified. Compounds 2 (IC50 = 11.05 μM) and 4 (IC50 = 43.54 μM) are thieno[2,3-b]pyridine derivatives that have the same scaffolds with a known eEF2K inhibitor, while compound 13 (IC50 = 70.13 μM) was a new thiophene-2-amine-type eEF2K inhibitor. Conclusions: CGBSP supplied an efficient strategy in the identification of novel eEF2K inhibitors and provided useful scaffolds for optimization. Full article
(This article belongs to the Special Issue Feature Papers in Cancer Biology and Anticancer Therapeutics)
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13 pages, 3012 KiB  
Article
A Unique Anti-Cancer 3-Styrylchromone Suppresses Inflammatory Response via HMGB1-RAGE Signaling
by Hideaki Abe, Miwa Okazawa, Takahiro Oyama, Hiroaki Yamazaki, Atsushi Yoshimori, Takanori Kamiya, Mitsutoshi Tsukimoto, Koichi Takao, Yoshiaki Sugita, Hiroshi Sakagami, Takehiko Abe and Sei-ichi Tanuma
Medicines 2021, 8(4), 17; https://doi.org/10.3390/medicines8040017 - 24 Mar 2021
Cited by 5 | Viewed by 4701
Abstract
Background: High mobility group box 1 (HMGB1)-receptor for advanced glycation endo-products (RAGE) axis serves as a key player in linking inflammation and carcinogenesis. Recently, papaverine was revealed to suppress the HMGB1-RAGE inflammatory signaling pathway and cancer cell proliferation. Therefore, a dual suppressor targeting [...] Read more.
Background: High mobility group box 1 (HMGB1)-receptor for advanced glycation endo-products (RAGE) axis serves as a key player in linking inflammation and carcinogenesis. Recently, papaverine was revealed to suppress the HMGB1-RAGE inflammatory signaling pathway and cancer cell proliferation. Therefore, a dual suppressor targeting this axis is expected to become a new type of therapeutic agent to treat cancer. Methods: Papaverine 3D pharmacophore mimetic compounds were selected by the LigandScout software from our in-house, anti-cancer chemical library and assessed for their anti-inflammatory activities by a HMGB1-RAGE-mediated interleukin-6 production assay using macrophage-like RAW264.7 cells. Molecular-biological analyses, such as Western blotting, were performed to clarify the mechanism of action. Results: A unique 6-methoxy-3-hydroxy-styrylchromone was found to possess potent anti-inflammatory and anti-cancer activities via the suppression of the HMGB1-RAGE-extracellular signal-regulated kinase 1/2 signaling pathway. Furthermore, the 3D pharmacophore-activity relationship analyses revealed that the hydroxyl group at the C4′ position of the benzene ring in a 3-styryl moiety was significant in its dual suppressive effects. Conclusions: These findings indicated that this compound may provide a valuable scaffold for the development of a new type of anti-cancer drug possessing anti-inflammatory activity and as a tool for understanding the link between inflammation and carcinogenesis. Full article
(This article belongs to the Special Issue Feature Papers in Cancer Biology and Anticancer Therapeutics)
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Review

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11 pages, 628 KiB  
Review
Role of Microbial Infection-Induced Inflammation in the Development of Gastrointestinal Cancers
by Keita Kouzu, Hironori Tsujimoto, Yoji Kishi, Hideki Ueno and Nariyoshi Shinomiya
Medicines 2021, 8(8), 45; https://doi.org/10.3390/medicines8080045 - 17 Aug 2021
Cited by 10 | Viewed by 4094
Abstract
There has been increasing evidence that a local inflammatory response stimulates tumor cells to acquire metastatic potential, and the concept of inflammatory oncotaxis has been spreading in recent years. However, the interaction between microbial inflammation and the development of gastrointestinal cancer is still [...] Read more.
There has been increasing evidence that a local inflammatory response stimulates tumor cells to acquire metastatic potential, and the concept of inflammatory oncotaxis has been spreading in recent years. However, the interaction between microbial inflammation and the development of gastrointestinal cancer is still unclear. This review summarizes the present knowledge on the role of microbial inflammation in the development of gastrointestinal cancers from the perspective of molecular biological findings. Chronic inflammation caused by bacterial infection is known to induce cancers as exemplified by Helicobacter pylori, which is associated with the development of gastric cancer via the activation of the TLR4 pathway by bacterial lipopolysaccharide followed by cancer growth through CagA-MET signaling. In addition, the development of inflammatory bowel diseases has been known to become a risk factor for colorectal cancers, where inflammation caused by certain bacterial infections plays a key role. It is also known that the cancer microenvironment is associated with cancer growth. Moreover, infectious complication after surgery for gastrointestinal cancers may promote tumor progression via the stimulation of pathogen-associated molecular patterns and various inflammatory mediators secreted by immunocytes. Further research on the link between microbial inflammation and cancer progression is needed to drive a paradigm shift in cancer treatment. Full article
(This article belongs to the Special Issue Feature Papers in Cancer Biology and Anticancer Therapeutics)
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