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Special Issue "Contribution of Cancer-Targeting Drugs toward Faster Clinical Application"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (30 September 2021).

Special Issue Editors

Prof. Dr. Sungpil Yoon
E-Mail Website
Guest Editor
School of Pharmacy, Sungkyunkwan University, Suwon, Korea
Interests: drug-resistant cancer; poor prognostic cancer; cancer metabolism; transcriptional regulation of cancer; drug repositioning; combination therapy; drugs for faster clinical application
Prof. Dr. Hyung Sik Kim
E-Mail Website
Guest Editor
School of Pharmacy, Sungkyunkwan University, Korea
Interests: drug-resistant cancer; poor prognostic cancer; cancer metabolism; transcriptional regulation of cancer; drug repositioning; combination therapy; drugs for faster clinical application

Special Issue Information

Dear Colleagues,

Various cancer-targeting drugs (synthesized small molecules, natural products, antibodies, etc.) have been developed; these include: 1. general chemotherapeutic drugs that inhibit cell division and growth, 2. specific protein-targeting drugs that block overexpressed growth signaling, the abnormal production of ATP energy, or cancer-generated angiogenesis, and 3. cellular immunotherapeutic drugs with an enhanced attack on cancer cells.

However, in many cases, cancer cells have developed resistance to current cancer-targeting drugs. Drug-resistant cancers (P-glycoprotein overexpression or mutations in the growth signaling pathways, apoptotic pathways, or repair system), metastatic cancers, advanced-stage cancers (e.g., ovarian or pancreatic), or stem cell-like cancers are difficult to treat using the currently available cancer-targeting drugs. Therefore, it is important to improve the existing drugs or generate novel therapeutic options to overcome the failure of current cancer-targeting drugs. Identifying the mechanisms or therapeutic options (single drug or combination therapy) for targeting cancer cells that would overcome the inefficiencies of current cancer-targeting drugs could lead to better treatment options for patients with cancers that are resistant to the available cancer-targeting drugs.

In this Research Topic, we aim to identify and investigate the novel applications of cancer-targeting drugs, including 1. products derived from original drugs, 2. drug repositioning, 3. experimental drugs soon to be available for testing in clinical trials, and 4. plant extracts or natural products. In our investigations, we also plan to include the pharmacokinetics and pharmacodynamics of combination drug treatments offering improvements over current therapies.

We expect that our findings will encourage the faster initiation of clinical trials as well as therapeutic application.

Prof. Dr. Sungpil Yoon
Prof. Dr. Hyung Sik Kim
Guest Editors

Manuscript Submission Information

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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

  • anti-cancer drug
  • chemotherapy
  • molecular targeting
  • immunotherapy
  • co-treatment
  • low toxicity
  • resistant cancer
  • metastasis
  • late stage cancer
  • cancer stem cell

Published Papers (4 papers)

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Research

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Article
Bazedoxifene, a GP130 Inhibitor, Modulates EMT Signaling and Exhibits Antitumor Effects in HPV-Positive Cervical Cancer
Int. J. Mol. Sci. 2021, 22(16), 8693; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168693 - 13 Aug 2021
Viewed by 345
Abstract
Persistent HPV (Human Papillomavirus) infection is the primary cause of cervical cancer. Despite the development of the HPV vaccine to prevent infections, cervical cancer is still a fatal malignant tumor and metastatic disease, and it is often difficult to treat, so a new [...] Read more.
Persistent HPV (Human Papillomavirus) infection is the primary cause of cervical cancer. Despite the development of the HPV vaccine to prevent infections, cervical cancer is still a fatal malignant tumor and metastatic disease, and it is often difficult to treat, so a new treatment strategy is needed. The FDA-approved drug Bazedoxifene is a novel inhibitor of protein–protein interactions between IL-6 and GP130. Multiple ligand simultaneous docking and drug repositioning approaches have demonstrated that an IL-6/GP130 inhibitor can act as a selective estrogen modulator. However, the molecular basis for GP130 activation in cervical cancer remains unclear. In this study, we investigated the anticancer properties of Bazedoxifene in HPV-positive cervical cancer cells. In vitro and in vivo experiments showed that Bazedoxifene inhibited cell invasion, migration, colony formation, and tumor growth in cervical cancer cells. We also confirmed that Bazedoxifene inhibits the GP130/STAT3 pathway and suppresses the EMT (Epithelial-mesenchymal transition) sub-signal. Thus, these data not only suggest a molecular mechanism by which the GP130/STAT3 pathway may promote cancer, but also may provide a basis for cervical cancer replacement therapy. Full article
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Article
Effects of the Anti-Tumorigenic Agent AT101 on Human Glioblastoma Cells in the Microenvironmental Glioma Stem Cell Niche
Int. J. Mol. Sci. 2021, 22(7), 3606; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073606 - 30 Mar 2021
Viewed by 558
Abstract
Glioblastoma (GBM) is a barely treatable disease due to its profound chemoresistance. A distinct inter- and intratumoral heterogeneity reflected by specialized microenvironmental niches and different tumor cell subpopulations allows GBMs to evade therapy regimens. Thus, there is an urgent need to develop alternative [...] Read more.
Glioblastoma (GBM) is a barely treatable disease due to its profound chemoresistance. A distinct inter- and intratumoral heterogeneity reflected by specialized microenvironmental niches and different tumor cell subpopulations allows GBMs to evade therapy regimens. Thus, there is an urgent need to develop alternative treatment strategies. A promising candidate for the treatment of GBMs is AT101, the R(-) enantiomer of gossypol. The present study evaluates the effects of AT101, alone or in combination with temozolomide (TMZ), in a microenvironmental glioma stem cell niche model of two GBM cell lines (U251MG and U87MG). AT101 was found to induce strong cytotoxic effects on U251MG and U87MG stem-like cells in comparison to the respective native cells. Moreover, a higher sensitivity against treatment with AT101 was observed upon incubation of native cells with a stem-like cell-conditioned medium. This higher sensitivity was reflected by a specific inhibitory influence on the p-p42/44 signaling pathway. Further, the expression of CXCR7 and the interleukin-6 receptor was significantly regulated upon these stimulatory conditions. Since tumor stem-like cells are known to mediate the development of tumor recurrences and were observed to strongly respond to the AT101 treatment, this might represent a promising approach to prevent the development of GBM recurrences. Full article
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Article
Loss of FADD and Caspases Affects the Response of T-Cell Leukemia Jurkat Cells to Anti-Cancer Drugs
Int. J. Mol. Sci. 2021, 22(5), 2702; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052702 - 07 Mar 2021
Viewed by 837
Abstract
Programmed cell death (PCD) pathways play a crucial role in the response of cancer cells to treatment. Their dysregulation is one of the cancer hallmarks and one of the reasons of drug resistance. Here, we studied the significance of the individual members of [...] Read more.
Programmed cell death (PCD) pathways play a crucial role in the response of cancer cells to treatment. Their dysregulation is one of the cancer hallmarks and one of the reasons of drug resistance. Here, we studied the significance of the individual members of PCD signaling pathways in response to treatment with common anti-cancer drugs using the T-cell leukemia Jurkat cells with single or double knockouts of necroptosis and/or apoptosis genes. We identified apoptosis as the primary cell death pathway upon anti-cancer drugs treatment. The cells with knocked out either Fas-associated protein with death domain (FADD) or all executioner caspases were resistant. This resistance could be partially overcome by induction of RIP1-dependent necroptosis through TNFR1 activation using combined treatment with TNF-α and smac mimetic (LCL161). RIP1 was essential for cellular response to TNF-α and smac mimetic, but dispensable for the response to anti-cancer drugs. Here, we demonstrated the significance of FADD and executioner caspases in carrying out programmed cell death upon anti-cancer drug treatments and the ability of combined treatment with TNF-α and smac mimetic to partially overcome drug resistance of FADD and/or CASP3/7/6-deficient cells via RIP1-dependent necroptosis. Thus, a combination of TNF-α and smac mimetic could be a suitable strategy for overcoming resistance to therapy in cells unable to trigger apoptosis. Full article
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Review

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Review
Synthetic Retinoids as Potential Therapeutics in Prostate Cancer—An Update of the Last Decade of Research: A Review
Int. J. Mol. Sci. 2021, 22(19), 10537; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910537 - 29 Sep 2021
Viewed by 278
Abstract
Prostate cancer (PC) is the second most common tumor in males. The search for appropriate therapeutic options against advanced PC has been in process for several decades. Especially after cessation of the effectiveness of hormonal therapy (i.e., emergence of castration-resistant PC), PC management [...] Read more.
Prostate cancer (PC) is the second most common tumor in males. The search for appropriate therapeutic options against advanced PC has been in process for several decades. Especially after cessation of the effectiveness of hormonal therapy (i.e., emergence of castration-resistant PC), PC management options have become scarce and the prognosis is poor. To overcome this stage of disease, an array of natural and synthetic substances underwent investigation. An interesting and promising class of compounds constitutes the derivatives of natural retinoids. Synthesized on the basis of the structure of retinoic acid, they present unique and remarkable properties that warrant their investigation as antitumor drugs. However, there is no up-to-date compilation that consecutively summarizes the current state of knowledge about synthetic retinoids with regard to PC. Therefore, in this review, we present the results of the experimental studies on synthetic retinoids conducted within the last decade. Our primary aim is to highlight the molecular targets of these compounds and to identify their potential promise in the treatment of PC. Full article
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