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Tumor Targeting Therapy and Selective Killing 2018
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Tumor Targeting Therapy and Selective Killing 2018

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (1 June 2018) | Viewed by 21893

Special Issue Editor

Prof. Dr. Hsueh-Wei Chang

E-Mail Website
Guest Editor
Department of Biomedical Science and Environmental Biology, College of Life Science, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Interests: natural product screening for anticancer; oxidative stress, antioxidant, DNA damage, apoptosis, selective killing, flow cytometry
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Tumor targeting therapies are drugs or other molecules that suppress cancer proliferation or metastasis by interacting with tumor-specific targets. To date, many tumor targeting therapies have been used in clinical cancer treatments, such as apoptosis inducers, hormone therapy, angiogenesis inhibitors, small molecule treatment, and antibody therapy. For example, cancer cells may have a tendency to escape apoptosis due to drug resistance; yet apoptosis inducers may improve the therapeutic effect of drugs by decreasing drug resistance. 

Tumor targeting therapies are expected to specifically target tumor cells and interact less with normal cells than most standard chemotherapy drugs. However, tumor targeting therapies are extremely intricate and not always effective when the target is absent from the tumor. Moreover, serious side effects or treatment resistances to tumor targeting therapies may randomly appear in certain patients. Therefore, current tumor targeting therapies still have some limitations.

Recently, the combinational treatments of different tumor targeting therapies or a tumor targeting therapy combined with one or more standard chemotherapy drug have caught our attention. Accordingly, more chosen targets may be helpful to improve therapeutic effects. Moreover, natural products, or novel small molecules with selective killing inhibition of tumor cells which are less toxic to normal cells, may be effective in tumor therapy when combining tumor targeting therapies. Some natural products potentially reduce the possible side effects of tumor targeting therapies.

This Special Issue on “Tumor Targeting Therapy and Selective Killing” will explore the impact of anticancer effects and its mechanisms of action as well as drug discoveries and novel combinational treatments.

We look forward to receiving reviews and original papers depicting all aspects of tumor targeting therapies and selective killing, including, but not limited to: Tumor targeting treatment, tumor targeting modulators, selective killing agents, selective killing modulators, apoptosis inducers, drug discovery, and natural products. We also aim to publish recent progress regarding molecular and pharmacologic aspects of this topic.

Prof. Dr. Hsueh-Wei Chang
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. 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

  • tumor targeting treatment
  • tumor targeting modulators
  • selective killing agents
  • selective killing modulators
  • apoptosis inducers
  • drug discovery
  • natural products
  • combinational treatment

Related Special Issue

Published Papers (5 papers)

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Research

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15 pages, 1374 KiB  
Article
Optimization of Early Steps in Oncolytic Adenovirus ONCOS-401 Production in T-175 and HYPERFlasks
by Lukasz Kuryk, Anne-Sophie W Møller, Antti Vuolanto, Sari Pesonen, Mariangela Garofalo, Vincenzo Cerullo and Magnus Jaderberg
Int. J. Mol. Sci. 2019, 20(3), 621; https://doi.org/10.3390/ijms20030621 - 31 Jan 2019
Cited by 15 | Viewed by 3656
Abstract
Oncolytic adenoviruses can trigger lysis of tumor cells, induce an antitumor immune response, bypass classical chemotherapeutic resistance strategies of tumors, and provide opportunities for combination strategies. A major challenge is the development of scalable production methods for viral seed stocks and sufficient quantities [...] Read more.
Oncolytic adenoviruses can trigger lysis of tumor cells, induce an antitumor immune response, bypass classical chemotherapeutic resistance strategies of tumors, and provide opportunities for combination strategies. A major challenge is the development of scalable production methods for viral seed stocks and sufficient quantities of clinical grade viruses. Because of promising clinical signals in a compassionate use program (Advanced Therapy Access Program) which supported further development, we chose the oncolytic adenovirus ONCOS-401 as a testbed for a new approach to scale up. We found that the best viral production conditions in both T-175 flasks and HYPERFlasks included A549 cells grown to 220,000 cells/cm2 (80% confluency), with ONCOS-401 infection at 30 multiplicity of infection (MOI), and an incubation period of 66 h. The Lysis A harvesting method with benzonase provided the highest viral yield from both T-175 and HYPERFlasks (10,887 ± 100 and 14,559 ± 802 infectious viral particles/cell, respectively). T-175 flasks and HYPERFlasks produced up to 2.1 × 109 ± 0.2 and 1.75 × 109 ± 0.08 infectious particles of ONCOS-401 per cm2 of surface area, respectively. Our findings suggest a suitable stepwise process that can be applied to optimizing the initial production of other oncolytic viruses. Full article
(This article belongs to the Special Issue Tumor Targeting Therapy and Selective Killing 2018)
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17 pages, 7919 KiB  
Article
Specific Antibody Fragment Ligand Traps Blocking FGF1 Activity
by Julia Chudzian, Anna Szlachcic, Malgorzata Zakrzewska, Miroslawa Czub, Marcin Pustula, Tad A. Holak and Jacek Otlewski
Int. J. Mol. Sci. 2018, 19(9), 2470; https://doi.org/10.3390/ijms19092470 - 21 Aug 2018
Cited by 5 | Viewed by 4568
Abstract
Fibroblast growth factor 1 (FGF1) and its receptors (FGFRs) regulate crucial biological processes such as cell proliferation and differentiation. Aberrant activation of FGFRs by their ligands can promote tumor growth and angiogenesis in many tumor types, including lung or breast cancer. The development [...] Read more.
Fibroblast growth factor 1 (FGF1) and its receptors (FGFRs) regulate crucial biological processes such as cell proliferation and differentiation. Aberrant activation of FGFRs by their ligands can promote tumor growth and angiogenesis in many tumor types, including lung or breast cancer. The development of FGF1-targeting molecules with potential implications for the therapy of FGF1-driven tumors is recently being considered a promising approach in the treatment of cancer. In this study we have used phage display selection to find scFv antibody fragments selectively binding FGF1 and preventing it from binding to its receptor. Three identified scFv clones were expressed and characterized with regard to their binding to FGF1 and ability to interfere with FGF1-induced signaling cascades activation. In the next step the scFvs were cloned to scFv-Fc format, as dimeric Fc fusions prove beneficial in prospective therapeutic application. As expected, scFvs-Fc exhibited significantly increased affinity towards FGF1. We observed strong antiproliferative activity of the scFvs and scFvs-Fc in the in vitro cell models. Presented antibody fragments serve as novel FGF1 inhibitors and can be further utilized as powerful tools to use in the studies on the selective cancer therapy. Full article
(This article belongs to the Special Issue Tumor Targeting Therapy and Selective Killing 2018)
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10 pages, 1805 KiB  
Article
Downregulations of AKT/mTOR Signaling Pathway for Salmonella-Mediated Suppression of Matrix Metalloproteinases-9 Expression in Mouse Tumor Models
by Yu-Tzu Tsao, Chun-Yu Kuo, Shun-Ping Cheng and Che-Hsin Lee
Int. J. Mol. Sci. 2018, 19(6), 1630; https://doi.org/10.3390/ijms19061630 - 31 May 2018
Cited by 28 | Viewed by 3654
Abstract
The roles of Matrix MetalloProteinases (MMPs), such as MMP-9, in tumor metastasis are well studied, and this in turns stimulates the development of MMP inhibitors as antitumor agents. Previously, Salmonella accumulation was observed in the metastatic nodules of the lungs after systemic administration. [...] Read more.
The roles of Matrix MetalloProteinases (MMPs), such as MMP-9, in tumor metastasis are well studied, and this in turns stimulates the development of MMP inhibitors as antitumor agents. Previously, Salmonella accumulation was observed in the metastatic nodules of the lungs after systemic administration. Salmonella significantly enhanced the survival of the pulmonary metastatic tumor-bearing mice. Based on our previous observation, we hypothesized that Salmonella could affect metastasis-related protein expression. The treatment of Salmonella clearly reduced the expression of MMP-9. Meanwhile, the MMP-9 related signaling pathways, including Phosph-Protein Kinase B (P-AKT) and Phosph-mammalian Targets Of Rapamycin (P-mTOR) were decreased after a Salmonella treatment. The Salmonella inhibited tumor cell migration by wound-healing and Transwell assay. The anti-metastatic effects of Salmonella were evaluated in mice bearing experimental metastasis tumor models. Consequently, Salmonella inhibited the expression of MMP-9 by reducing the AKT/mTOR pathway and metastatic nodules in vivo. Full article
(This article belongs to the Special Issue Tumor Targeting Therapy and Selective Killing 2018)
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17 pages, 5976 KiB  
Article
Erythropoietin Intensifies the Proapoptotic Activity of LFM-A13 in Cells and in a Mouse Model of Colorectal Cancer
by Anna Tankiewicz-Kwedlo, Justyna Magdalena Hermanowicz, Krystyna Pawlak, Robert Czarnomysy, Krzysztof Bielawski, Izabela Prokop and Dariusz Pawlak
Int. J. Mol. Sci. 2018, 19(4), 1262; https://doi.org/10.3390/ijms19041262 - 23 Apr 2018
Cited by 4 | Viewed by 4196
Abstract
The Bruton’s tyrosine kinase (BTK) inhibitor LFM-A13 has been widely employed as an antileukemic agent, but applications in solid cancer have been found recently. The compound promotes apoptosis, has an antiproliferative effect, and increases cancer cell sensitivity to chemotherapy drugs. We decided to [...] Read more.
The Bruton’s tyrosine kinase (BTK) inhibitor LFM-A13 has been widely employed as an antileukemic agent, but applications in solid cancer have been found recently. The compound promotes apoptosis, has an antiproliferative effect, and increases cancer cell sensitivity to chemotherapy drugs. We decided to assess the impact of the simultaneous use of erythropoietin (Epo) and LFM-A13 on signal transduction in colon DLD-1 and HT-29 cells, as well as in tumor xenografts. The induction of apoptosis by Epo and LFM-A-13 in the cells was confirmed by phosphatidylserine externalization, loss of mitochondrial membrane potential, and modulation of the expression of apoptotic protein BAX and antiapoptotic protein BCL-2 in colon adenocarcinoma cells. Nude mice were inoculated with adenocarcinoma cells and treated with Epo and LFM-A13 in order to evaluate the degree of tumor regression. The simultaneous use of Epo and LFM-A13 severely inhibited cell growth, activated apoptosis, and also inhibited tumor growth in xenografts. The addition of Epo to LFM-A13 intensified the antiproliferative effect of LFM-A13, confirmed by the loss of mitochondrial membrane potential and the accumulation of apoptotic colon cancer cells with externalized phosphatidylserine (PS). These preclinical results suggest that the combination of Epo and LFM-A13 has a high proapoptotic activity and should be tested in the clinic for the treatment of solid tumors such as colon cancer. Full article
(This article belongs to the Special Issue Tumor Targeting Therapy and Selective Killing 2018)
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Review

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11 pages, 929 KiB  
Review
Mechanisms of Tumor Growth Inhibition by Depletion of γ-Glutamylcyclotransferase (GGCT): A Novel Molecular Target for Anticancer Therapy
by Susumu Kageyama, Hiromi Ii, Keiko Taniguchi, Shigehisa Kubota, Tetsuya Yoshida, Takahiro Isono, Tokuhiro Chano, Taku Yoshiya, Kosei Ito, Tatsuhiro Yoshiki, Akihiro Kawauchi and Susumu Nakata
Int. J. Mol. Sci. 2018, 19(7), 2054; https://doi.org/10.3390/ijms19072054 - 14 Jul 2018
Cited by 30 | Viewed by 5239
Abstract
γ-Glutamylcyclotransferase (GGCT), which is one of the major enzymes involved in glutathione metabolism, is upregulated in a wide range of cancers—glioma, breast, lung, esophageal, gastric, colorectal, urinary bladder, prostate, cervical, ovarian cancers and osteosarcoma—and promotes cancer progression; its depletion leads to the suppression [...] Read more.
γ-Glutamylcyclotransferase (GGCT), which is one of the major enzymes involved in glutathione metabolism, is upregulated in a wide range of cancers—glioma, breast, lung, esophageal, gastric, colorectal, urinary bladder, prostate, cervical, ovarian cancers and osteosarcoma—and promotes cancer progression; its depletion leads to the suppression of proliferation, invasion, and migration of cancer cells. It has been demonstrated that the suppression or inhibition of GGCT has an antitumor effect in cancer-bearing xenograft mice. Based on these observations, GGCT is now recognized as a promising therapeutic target in various cancers. This review summarizes recent advances on the mechanisms of the antitumor activity of GGCT inhibition. Full article
(This article belongs to the Special Issue Tumor Targeting Therapy and Selective Killing 2018)
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