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Molecules
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Targeting of Signaling Pathways for Cancer Therapy, 2nd Edition
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Targeting of Signaling Pathways for Cancer Therapy, 2nd Edition

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 11127

Special Issue Editors

Prof. Dr. Sergei Boichuk

E-Mail Website
Guest Editor
Department of Pathology, Kazan State Medical University, Kazan, Russia
Interests: cancer, gastrointestinal stromal tumors (GIST); soft tissue sarcomas (STS); targeted-based therapy; resistance; apoptosis; receptor tyrosine kinase inhibitors (RTKi); DNA damage repair (DDR); FGF-signaling
Special Issues, Collections and Topics in MDPI journals
Dr. Gülçin Tezcan

E-Mail Website
Guest Editor
Department of Fundamental Sciences, Faculty of Dentistry, Bursa Uludag University, 16059 Bursa, Turkey
Interests: immune response; cytotoxic T cells; cytokines; inflammasome; molecular regulation of inflammasome; cancer pathogenesis

Special Issue Information

Dear Colleagues,

Cell-signaling pathways are well-known regulators of cell growth, proliferation, migration, differentiation, and survival. Several signaling pathways have been identified as frequently genetically altered in cancer, including the p53-signaling pathway, RTK/RAS/MAP-kinase and PI3K/AKT signaling pathway, Notch and Wnt signaling pathways, GSK3-signaling pathway, actin dynamics signaling pathway, death receptor signaling pathway, autophagy pathway, and others. For example, the activation of some of the pathways indicated above might be due to activating mutations of RTKs, Ras, PI3k, Akt, etc., or the loss of function of tumor suppressors (e.g., Pten). Given that signal transduction in these pathways is tightly regulated by protein kinases, and taking into account that several of the cell membrane receptor families activate the same downstream intracellular pathways, the development of a specific kinase or other receptor inhibitors targeting the universal signaling molecules is considered as one of the most promising approaches for personalized therapies for cancers that are addicted to a particular signaling pathway.

Prof. Dr. Sergei Boichuk
Dr. Gülçin Tezcan
Guest Editors

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. Molecules is an international peer-reviewed open access semimonthly 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 2700 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
  • receptor tyrosine kinase
  • cell death
  • small molecule inhibitors
  • bioactive molecules
  • nano molecules
  • personalized therapy
  • cell therapy

Related Special Issue

Published Papers (4 papers)

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Research

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12 pages, 1861 KiB  
Article
Extended-Synaptotagmin 1 Enhances Liver Cancer Progression Mediated by the Unconventional Secretion of Cytosolic Proteins
by Kohji Yamada, Yoshito Hannya, Tsunekazu Oikawa, Ayano Yoshida, Kuniko Katagiri, Saishu Yoshida, Rei Koizumi, Naoko Tago, Yuya Shimoyama, Akira Kawamura, Yuta Mochimaru, Ken Eto and Kiyotsugu Yoshida
Molecules 2023, 28(10), 4033; https://doi.org/10.3390/molecules28104033 - 11 May 2023
Cited by 2 | Viewed by 1855
Abstract
Extended-synaptotagmin 1 (E-Syt1) is an endoplasmic reticulum membrane protein that is involved in cellular lipid transport. Our previous study identified E-Syt1 as a key factor for the unconventional protein secretion of cytoplasmic proteins in liver cancer, such as protein kinase C delta (PKCδ); [...] Read more.
Extended-synaptotagmin 1 (E-Syt1) is an endoplasmic reticulum membrane protein that is involved in cellular lipid transport. Our previous study identified E-Syt1 as a key factor for the unconventional protein secretion of cytoplasmic proteins in liver cancer, such as protein kinase C delta (PKCδ); however, it is unclear whether E-Syt1 is involved in tumorigenesis. Here, we showed that E-Syt1 contributes to the tumorigenic potential of liver cancer cells. E-Syt1 depletion significantly suppressed the proliferation of liver cancer cell lines. Database analysis revealed that E-Syt1 expression is a prognostic factor for hepatocellular carcinoma (HCC). Immunoblot analysis and cell-based extracellular HiBiT assays showed that E-Syt1 was required for the unconventional secretion of PKCδ in liver cancer cells. Furthermore, deficiency of E-Syt1 suppressed the activation of insulin-like growth factor 1 receptor (IGF1R) and extracellular-signal-related kinase 1/2 (Erk1/2), both of which are signaling pathways mediated by extracellular PKCδ. Three-dimensional sphere formation and xenograft model analysis revealed that E-Syt1 knockout significantly decreased tumorigenesis in liver cancer cells. These results provide evidence that E-Syt1 is critical for oncogenesis and is a therapeutic target for liver cancer. Full article
(This article belongs to the Special Issue Targeting of Signaling Pathways for Cancer Therapy, 2nd Edition)
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Review

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23 pages, 2986 KiB  
Review
Immunomodulatory Gene-Splicing Dysregulation in Tumorigenesis: Unmasking the Complexity
by Lorraine Tshegofatso Maebele, Thanyani Victor Mulaudzi, Madhavan Yasasve, Zodwa Dlamini and Botle Precious Damane
Molecules 2023, 28(16), 5984; https://doi.org/10.3390/molecules28165984 - 10 Aug 2023
Cited by 1 | Viewed by 1391
Abstract
Cancer is a global health concern with rising incidence, morbidity, and mortality. The interaction between the tumor and immune cells within the tumor microenvironment is facilitated by signaling pathways driven by immunomodulatory proteins. Alternative splicing regulates the production of multiple immunomodulatory proteins with [...] Read more.
Cancer is a global health concern with rising incidence, morbidity, and mortality. The interaction between the tumor and immune cells within the tumor microenvironment is facilitated by signaling pathways driven by immunomodulatory proteins. Alternative splicing regulates the production of multiple immunomodulatory proteins with diverse functionality from a single mRNA transcript. Splicing factors are pivotal in modulating alternative splicing processes but are also subject to regulation. The dysregulation of alternative splicing may result from splicing factor (SF) abnormal expression levels and mutations in the cis and trans-acting elements and small nuclear RNA (snRNA) molecules. Aberrant splicing may generate abnormal mRNA transcripts encoding isoforms with altered functions that contribute to tumorigenesis or cancer progression. This review uncovers the complexity of immunomodulatory genes splicing dysregulation in oncogenesis. Identifying specific immunomodulatory splicing isoforms that contribute to cancer could be utilized to improve current immunotherapeutic drugs or develop novel therapeutic interventions for cancer. Full article
(This article belongs to the Special Issue Targeting of Signaling Pathways for Cancer Therapy, 2nd Edition)
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20 pages, 2188 KiB  
Review
Antitumor Activity of s-Triazine Derivatives: A Systematic Review
by Qiuzi Dai, Qinsheng Sun, Xiaorong Ouyang, Jinyang Liu, Liye Jin, Ahao Liu, Binsheng He, Tingting Fan and Yuyang Jiang
Molecules 2023, 28(11), 4278; https://doi.org/10.3390/molecules28114278 - 23 May 2023
Cited by 8 | Viewed by 2709
Abstract
1,3,5-triazine derivatives, also called s-triazines, are a series of containing-nitrogen heterocyclic compounds that play an important role in anticancer drug design and development. To date, three s-triazine derivatives, including altretamine, gedatolisib, and enasidenib, have already been approved for refractory ovarian cancer, metastatic breast [...] Read more.
1,3,5-triazine derivatives, also called s-triazines, are a series of containing-nitrogen heterocyclic compounds that play an important role in anticancer drug design and development. To date, three s-triazine derivatives, including altretamine, gedatolisib, and enasidenib, have already been approved for refractory ovarian cancer, metastatic breast cancer, and leukemia therapy, respectively, demonstrating that the s-triazine core is a useful scaffold for the discovery of novel anticancer drugs. In this review, we mainly focus on s-triazines targeting topoisomerases, tyrosine kinases, phosphoinositide 3-kinases, NADP+-dependent isocitrate dehydrogenases, and cyclin-dependent kinases in diverse signaling pathways, which have been extensively studied. The medicinal chemistry of s-triazine derivatives as anticancer agents was summarized, including discovery, structure optimization, and biological applications. This review will provide a reference to inspire new and original discoveries. Full article
(This article belongs to the Special Issue Targeting of Signaling Pathways for Cancer Therapy, 2nd Edition)
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16 pages, 1074 KiB  
Review
Rac1: A Regulator of Cell Migration and a Potential Target for Cancer Therapy
by Ning Ma, Erqian Xu, Qing Luo and Guanbin Song
Molecules 2023, 28(7), 2976; https://doi.org/10.3390/molecules28072976 - 27 Mar 2023
Cited by 11 | Viewed by 4161
Abstract
Cell migration is crucial for physiological and pathological processes such as morphogenesis, wound repair, immune response and cancer invasion/metastasis. There are many factors affecting cell migration, and the regulatory mechanisms are complex. Rac1 is a GTP-binding protein with small molecular weight belonging to [...] Read more.
Cell migration is crucial for physiological and pathological processes such as morphogenesis, wound repair, immune response and cancer invasion/metastasis. There are many factors affecting cell migration, and the regulatory mechanisms are complex. Rac1 is a GTP-binding protein with small molecular weight belonging to the Rac subfamily of the Rho GTPase family. As a key molecule in regulating cell migration, Rac1 participates in signal transduction from the external cell to the actin cytoskeleton and promotes the establishment of cell polarity which plays an important role in cancer cell invasion/metastasis. In this review, we firstly introduce the molecular structure and activity regulation of Rac1, and then summarize the role of Rac1 in cancer invasion/metastasis and other physiological processes. We also discuss the regulatory mechanisms of Rac1 in cell migration and highlight it as a potential target in cancer therapy. Finally, the current state as well as the future challenges in this area are considered. Understanding the role and the regulatory mechanism of Rac1 in cell migration can provide fundamental insights into Rac1-related cancer progression and further help us to develop novel intervention strategies for cancer therapy in clinic. Full article
(This article belongs to the Special Issue Targeting of Signaling Pathways for Cancer Therapy, 2nd Edition)
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