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Cell Signaling in Cancer Therapy
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Cell Signaling in Cancer Therapy

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

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 16597

Special Issue Editor

Prof. Dr. Luca Tamagnone

E-Mail Website
Guest Editor
Dipartimento di Scienze della Vita e Sanità Pubblica, Univesità Cattolica del Sacro Cuore, 00168 Roma, Italy
Interests: semaphorin; plexin; neuropilin; cancer; cell signaling; cell migration; metastasis; receptor

Special Issue Information

Dear Colleagues,

Although knowledge about the molecular mechanisms at the base of cancer development continues to grow, therapeutic regimens applied in the clinic have taken several years (if not decades) to evolve and include novel molecular-targeted approaches. Our current concept of cancer treatment is finally taking these innovative drugs into notable account, while the rapid and continued progress of translational research keeps unveiling relevant aspects of this complex disease. New cancer therapies have emerged from the understanding of tumor vulnerabilities and dependence on specific signaling pathways supporting growth and immune system evasion. Yet, cancer cell resilience and the evolving nature of tumor cell populations enable the onset of resistance to therapeutic attacks, which continues to challenge scientists to seek better ways to clutch the pivotal switches of the disease.

In this Special Issue, we would like to host reports of novel findings as well as reviews of the current knowledge concerning the cellular mechanisms relevant for cancer therapy. This comprises a broad range of research fields, from genetics to pharmacogenomics, from cancer cell biology to immunology, and from biochemistry to animal models and clinical studies.

A non-exhaustive list of potential topics includes the following:

  • Novel mechanisms of action of anti-cancer drugs;
  • Molecular mechanisms of resistance to cancer therapies;
  • New molecular targets and active molecules for cancer therapy;
  • New predictive biomarkers of responsiveness to cancer therapies;
  • Cell-derived and blood-borne biomarkers of therapeutic response/relapse;
  • Genetic and non-genetic mechanisms of cancer cell vulnerability;
  • Cancer stem cells and resistance to therapy;
  • Cell–cell signaling and tumor microenvironment targeting for cancer therapy

Prof. Dr. Luca Tamagnone
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

  • cell signaling
  • cancer
  • target therapy
  • cancer genetics
  • pharmacogenomics
  • resistance to therapy
  • metabolism
  • cancer stem cell
  • tumor microenvironment
  • angiogenesis
  • macrophages
  • immune response
  • immunotherapy
  • animal models

Published Papers (4 papers)

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Research

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17 pages, 3998 KiB  
Article
Expression of p53 Protein Associates with Anti-PD-L1 Treatment Response on Human-Derived Xenograft Model of GATA3/CR5/6-Negative Recurrent Nonmuscular Invasive Bladder Urothelial Carcinoma
by Ekaterina Blinova, Elena Samishina, Olga Deryabina, Dmitry Blinov, Dmitry Roshchin, Evgeniia Shich, Oxana Tumutolova, Ilya Fedoseykin, Anna Epishkina, Haydar Barakat, Andrey Kaprin, Kirill Zhandarov, Dmitrij Perepechin, Dmitrij Merinov, Gordey Brykin, Karen Arutiunian, Stanislav Serebrianyi, Artem Mirontsev and Andrew Kozdoba
Int. J. Mol. Sci. 2021, 22(18), 9856; https://doi.org/10.3390/ijms22189856 - 12 Sep 2021
Cited by 3 | Viewed by 2170
Abstract
Background: The possible involvement of p53 signaling, FGFR3 expression, and FGFR3 mutation rates in the prediction of the NMIBC anti-PD-L1 treatment response needs to be clarified. The main aim of our study was to explore predictive value of p53 expression, FGFR3 expression, and [...] Read more.
Background: The possible involvement of p53 signaling, FGFR3 expression, and FGFR3 mutation rates in the prediction of the NMIBC anti-PD-L1 treatment response needs to be clarified. The main aim of our study was to explore predictive value of p53 expression, FGFR3 expression, and its gene mutation status for the therapeutic success of anti-PD-L1 treatment in the patient-derived murine model of recurrent high-PD-L1(+) GATA3(−)/CR5/6(−) high-grade and low-grade NMIBC. Methods: twenty lines of patient-derived xenografts (PDXs) of relapsed high-PD-L1(+) double-negative NMIBC were developed, of which 10 lines represented high-grade tumors and the other ones—low-grade bladder cancer. Acceptors of each grade-related branch received specific anti-PD-L1 antibodies. Animals’ survival, tumor-doubling time, and remote metastasis were followed during the post-interventional period. PD-L1, GATA3, CR5/6, and p53 protein expressions in engrafted tumors were assessed by immunohistochemistry. The FGFR3 expression and FGFR3 mutations in codons 248 and 249 were detected by real-time polymerase chain reaction. Results: The expression of p53 protein is an independent factor affecting the animals’ survival time [HR = 0.036, p = 0.031] of anti-PD-L1-treated mice with low-grade high-PD-L1(+) double-negative NMIBC PDX. The FGFR3 expression and FGFR3 mutation rate have no impact on the anti-PD-L1 treatment response in the interventional groups. Conclusions: p53 expression may be considered as a prognostic factor for the anti-PD-L1 treatment efficacy of low-grade high-PD-L1-positive GATA3(−)/CR5/6(−)-relapsed noninvasive bladder cancer. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer Therapy)
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15 pages, 6742 KiB  
Article
Deficiency of NEIL3 Enhances the Chemotherapy Resistance of Prostate Cancer
by Yiwei Wang, Liuyue Xu, Shanshan Shi, Sha Wu, Ruijie Meng, Huifang Chen and Zhenyou Jiang
Int. J. Mol. Sci. 2021, 22(8), 4098; https://doi.org/10.3390/ijms22084098 - 15 Apr 2021
Cited by 16 | Viewed by 2439
Abstract
Acquired treatment resistance is an important cause of death in prostate cancer, and this study aimed to explore the mechanisms of chemotherapy resistance in prostate cancer. We employed castration-resistant prostate cancer (CRPC), neuroendocrine prostate cancer (NEPC), and chemotherapy-resistant prostate cancer datasets to screen [...] Read more.
Acquired treatment resistance is an important cause of death in prostate cancer, and this study aimed to explore the mechanisms of chemotherapy resistance in prostate cancer. We employed castration-resistant prostate cancer (CRPC), neuroendocrine prostate cancer (NEPC), and chemotherapy-resistant prostate cancer datasets to screen for potential target genes. The Cancer Genome Atlas (TCGA) was used to detect the correlation between the target genes and prognosis and clinical characteristics. Nei endonuclease VIII-like 3 (NEIL3) knockdown cell lines were constructed with RNA interference. Prostate cancer cells were treated with enzalutamide for the androgen deprivation therapy (ADT) model, and with docetaxel and cisplatin for the chemotherapy model. Apoptosis and the cell cycle were examined using flow cytometry. RNA sequencing and western blotting were performed in the knockdown Duke University 145 (DU145) cell line to explore the possible mechanisms. The TCGA dataset demonstrated that high NEIL3 was associated with a high T stage and Gleason score, and indicated a possibility of lymph node metastasis, but a good prognosis. The cell therapy models showed that the loss of NEIL3 could promote the chemotherapy resistance (but not ADT resistance) of prostate cancer (PCa). Flow cytometry revealed that the loss of NEIL3 in PCa could inhibit cell apoptosis and cell cycle arrest under cisplatin treatment. RNA sequencing showed that the knockdown of NEIL3 changes the expression of neuroendocrine-related genes. Further western blotting revealed that the loss of NEIL3 could significantly promote the phosphorylation of ATR serine/threonine kinase (ATR) and ATM serine/threonine kinase (ATM) under chemotherapy, thus initiating downstream pathways related to DNA repair. In summary, the loss of NEIL3 promotes chemotherapy resistance in prostate cancer, and NEIL3 may serve as a diagnostic marker for chemotherapy-resistant patients. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer Therapy)
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13 pages, 2541 KiB  
Article
Immunohistochemical Analysis of DNA Repair- and Drug-Efflux-Associated Molecules in Tumor and Peritumor Areas of Glioblastoma
by Cristiana Angelucci, Alessio D’Alessio, Silvia Sorrentino, Filippo Biamonte, Umberto Moscato, Annunziato Mangiola, Gigliola Sica and Fortunata Iacopino
Int. J. Mol. Sci. 2021, 22(4), 1620; https://doi.org/10.3390/ijms22041620 - 5 Feb 2021
Cited by 2 | Viewed by 2132
Abstract
Glioblastoma (GBM), the most commonly occurring primary tumor arising within the central nervous system, is characterized by high invasiveness and poor prognosis. In spite of the improvement in surgical techniques, along with the administration of chemo- and radiation therapy and the incessant investigation [...] Read more.
Glioblastoma (GBM), the most commonly occurring primary tumor arising within the central nervous system, is characterized by high invasiveness and poor prognosis. In spite of the improvement in surgical techniques, along with the administration of chemo- and radiation therapy and the incessant investigation in search of prospective therapeutic targets, the local recurrence that frequently occurs within the peritumoral brain tissue makes GBM the most malignant and terminal type of astrocytoma. In the current study, we investigated both GBM and peritumoral tissues obtained from 55 hospitalized patients and the expression of three molecules involved in the onset of resistance/unresponsiveness to chemotherapy: O6-methylguanine methyltransferase (MGMT), breast cancer resistance protein (BCRP1), and A2B5. We propose that the expression of these molecules in the peritumoral tissue might be crucial to promoting the development of early tumorigenic events in the tissue surrounding GBM as well as responsible for the recurrence originating in this apparently normal area and, accordingly, for the resistance to treatment with the standard chemotherapeutic regimen. Notably, the inverse correlation found between MGMT expression in peritumoral tissue and patients’ survival suggests a prognostic role for this protein. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer Therapy)
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Review

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22 pages, 756 KiB  
Review
Therapeutic Targeting of the Gas6/Axl Signaling Pathway in Cancer
by Mai Tanaka and Dietmar W. Siemann
Int. J. Mol. Sci. 2021, 22(18), 9953; https://doi.org/10.3390/ijms22189953 - 15 Sep 2021
Cited by 32 | Viewed by 8972
Abstract
Many signaling pathways are dysregulated in cancer cells and the host tumor microenvironment. Aberrant receptor tyrosine kinase (RTK) pathways promote cancer development, progression, and metastasis. Hence, numerous therapeutic interventions targeting RTKs have been actively pursued. Axl is an RTK that belongs to the [...] Read more.
Many signaling pathways are dysregulated in cancer cells and the host tumor microenvironment. Aberrant receptor tyrosine kinase (RTK) pathways promote cancer development, progression, and metastasis. Hence, numerous therapeutic interventions targeting RTKs have been actively pursued. Axl is an RTK that belongs to the Tyro3, Axl, MerTK (TAM) subfamily. Axl binds to a high affinity ligand growth arrest specific 6 (Gas6) that belongs to the vitamin K-dependent family of proteins. The Gas6/Axl signaling pathway has been implicated to promote progression, metastasis, immune evasion, and therapeutic resistance in many cancer types. Therapeutic agents targeting Gas6 and Axl have been developed, and promising results have been observed in both preclinical and clinical settings when such agents are used alone or in combination therapy. This review examines the current state of therapeutics targeting the Gas6/Axl pathway in cancer and discusses Gas6- and Axl-targeting agents that have been evaluated preclinically and clinically. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer Therapy)
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