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Cancers
Special Issues
Cell Signaling in Cancer and Cancer Therapy
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Cell Signaling in Cancer and Cancer Therapy

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 14569

Special Issue Editors

Prof. Dr. Zhixiang Wang

E-Mail Website
Guest Editor
Signal Transduction Research Group, Department of Medical Genetics, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada
Interests: receptor tyrosine kinases; EGFR; signal transduction; cancer therapy; breast cancer treatment; targeted therapy
Special Issues, Collections and Topics in MDPI journals
Dr. Yi Wang

E-Mail Website1 Website2
Guest Editor
1. Canadian Nuclear Laboratories, Chalk River, ON, Canada
2. Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada
Interests: cancer therapy; radiation therapy; targeted therapy; immune checkpoint therapy; low dose radiation; hypoxia; microenvironment; cell signaling; radiation protection; biodosimetry; high-throughput analysis; artificial intelligence and machine learning
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is driven by genetic and epigenetic modifications to enable cells to over-proliferate and escape from cell death. One hallmark of cancer is the aberrant cell signaling which is caused by the dysregulation of signaling proteins. Cell signaling plays a prominent role in regulating cell growth and division, cell death, cell fate, and cell motility. In a wider context, the microenvironment, angiogenesis, and inflammation are also governed by external and internal signals. These signals are transmitted in a highly intricate and tightly controlled manner through a series of signaling proteins. Hyperactivation or dysregulation of these signaling pathways, for example, PI3K-Akt and Ras-ERK pathways, can result in transformation of cellular proto-oncogenes to oncogenes. On the other hand, the inactivation of tumor suppressors eliminates important negative regulators of signaling, which results in uncontrolled cell proliferation and subsequent tumor development. The knowledge of cellular signal transduction pathways will be essential to understand the evolution of a pathological condition and the delicate balance that regulates cellular homeostasis.

Recently, targeting the component of cell signaling (either at cells such as targeted therapy or at microenvironment such as immune therapy) in cancer has emerged as the most prominent aspect of cancer treatment. In order to specially design novel drugs that intervene at dysregulated signaling nodes or repair missing signaling molecules, it is crucial to understand how oncogenic signaling pathways control the development of cancer.

In this Special Issue, we invite all papers that study the cell signaling underlying any aspects of cancer development. Research on the signaling pathway behind cancer therapies including targeted, immune, radiation and chemo-therapy are also welcomed. This Special Issue invites both original research articles as well as reviews, commentaries, and perspectives that cover all aspects of signal transduction.

Prof. Dr. Zhixiang Wang
Dr. Yi Wang
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 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. Cancers 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 2900 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

  • cell signaling
  • signal transduction
  • cancer therapy
  • radiation therapy
  • immune therapy
  • targeted therapy
  • chemotherapy
  • cell proliferation
  • cell death
  • cell motility

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Published Papers (6 papers)

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Research

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21 pages, 10695 KiB  
Article
Sulfamoylated Estradiol Analogs Targeting the Actin and Microtubule Cytoskeletons Demonstrate Anti-Cancer Properties In Vitro and In Ovo
by Anne Elisabeth Mercier, Anna Margaretha Joubert, Renaud Prudent, Jean Viallet, Agnes Desroches-Castan, Leanne De Koning, Peace Mabeta, Jolene Helena, Michael Sean Pepper and Laurence Lafanechère
Cancers 2024, 16(17), 2941; https://doi.org/10.3390/cancers16172941 - 23 Aug 2024
Cited by 1 | Viewed by 1126
Abstract
The microtubule-disrupting agent 2-methoxyestradiol (2-ME) displays anti-tumor and anti-angiogenic properties, but its clinical development is halted due to poor pharmacokinetics. We therefore designed two 2-ME analogs in silico—an ESE-15-one and an ESE-16 one—with improved pharmacological properties. We investigated the effects of these compounds [...] Read more.
The microtubule-disrupting agent 2-methoxyestradiol (2-ME) displays anti-tumor and anti-angiogenic properties, but its clinical development is halted due to poor pharmacokinetics. We therefore designed two 2-ME analogs in silico—an ESE-15-one and an ESE-16 one—with improved pharmacological properties. We investigated the effects of these compounds on the cytoskeleton in vitro, and their anti-angiogenic and anti-metastatic properties in ovo. Time-lapse fluorescent microscopy revealed that sub-lethal doses of the compounds disrupted microtubule dynamics. Phalloidin fluorescent staining of treated cervical (HeLa), metastatic breast (MDA-MB-231) cancer, and human umbilical vein endothelial cells (HUVECs) displayed thickened, stabilized actin stress fibers after 2 h, which rearranged into a peripheral radial pattern by 24 h. Cofilin phosphorylation and phosphorylated ezrin/radixin/moesin complexes appeared to regulate this actin response. These signaling pathways overlap with anti-angiogenic, extra-cellular communication and adhesion pathways. Sub-lethal concentrations of the compounds retarded both cellular migration and invasion. Anti-angiogenic and extra-cellular matrix signaling was evident with TIMP2 and P-VEGF receptor-2 upregulation. ESE-15-one and ESE-16 exhibited anti-tumor and anti-metastatic properties in vivo, using the chick chorioallantoic membrane assay. In conclusion, the sulfamoylated 2-ME analogs displayed promising anti-tumor, anti-metastatic, and anti-angiogenic properties. Future studies will assess the compounds for myeloproliferative effects, as seen in clinical applications of other drugs in this class. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer and Cancer Therapy)
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24 pages, 10914 KiB  
Article
The Tumor Suppressor SOCS1 Diminishes Tolerance to Oxidative Stress in Hepatocellular Carcinoma
by Akhil Shukla, Md Gulam Musawwir Khan, Anny Armas Cayarga, Mozhdeh Namvarpour, Mohammad Mobarak H. Chowdhury, Dominique Levesque, Jean-François Lucier, François-Michel Boisvert, Sheela Ramanathan and Subburaj Ilangumaran
Cancers 2024, 16(2), 292; https://doi.org/10.3390/cancers16020292 - 10 Jan 2024
Cited by 2 | Viewed by 1667
Abstract
SOCS1 is a tumor suppressor in hepatocellular carcinoma (HCC). Recently, we showed that a loss of SOCS1 in hepatocytes promotes NRF2 activation. Here, we investigated how SOCS1 expression in HCC cells affected oxidative stress response and modulated the cellular proteome. Murine Hepa1-6 cells [...] Read more.
SOCS1 is a tumor suppressor in hepatocellular carcinoma (HCC). Recently, we showed that a loss of SOCS1 in hepatocytes promotes NRF2 activation. Here, we investigated how SOCS1 expression in HCC cells affected oxidative stress response and modulated the cellular proteome. Murine Hepa1-6 cells expressing SOCS1 (Hepa-SOCS1) or control vector (Hepa-Vector) were treated with cisplatin or tert-butyl hydroperoxide (t-BHP). The induction of NRF2 and its target genes, oxidative stress, lipid peroxidation, cell survival and cellular proteome profiles were evaluated. NRF2 induction was significantly reduced in Hepa-SOCS1 cells. The gene and protein expression of NRF2 targets were differentially induced in Hepa-Vector cells but markedly suppressed in Hepa-SOCS1 cells. Hepa-SOCS1 cells displayed an increased induction of reactive oxygen species but reduced lipid peroxidation. Nonetheless, Hepa-SOCS1 cells treated with cisplatin or t-BHP showed reduced survival. GCLC, poorly induced in Hepa-SOCS1 cells, showed a strong positive correlation with NFE2L2 and an inverse correlation with SOCS1 in the TCGA-LIHC transcriptomic data. A proteomic analysis of Hepa-Vector and Hepa-SOCS1 cells revealed that SOCS1 differentially modulated many proteins involved in diverse molecular pathways, including mitochondrial ROS generation and ROS detoxification, through peroxiredoxin and thioredoxin systems. Our findings indicate that maintaining sensitivity to oxidative stress is an important tumor suppression mechanism of SOCS1 in HCC. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer and Cancer Therapy)
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Review

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27 pages, 4091 KiB  
Review
Unraveling Cancer’s Wnt Signaling: Dynamic Control through Protein Kinase Regulation
by Deniz Tümen, Philipp Heumann, Julia Huber, Nele Hahn, Celina Macek, Martha Ernst, Arne Kandulski, Claudia Kunst and Karsten Gülow
Cancers 2024, 16(15), 2686; https://doi.org/10.3390/cancers16152686 - 28 Jul 2024
Viewed by 1883
Abstract
Since the initial identification of oncogenic Wnt in mice and Drosophila, the Wnt signaling pathway has been subjected to thorough and extensive investigation. Persistent activation of Wnt signaling exerts diverse cancer characteristics, encompassing tumor initiation, tumor growth, cell senescence, cell death, differentiation, and [...] Read more.
Since the initial identification of oncogenic Wnt in mice and Drosophila, the Wnt signaling pathway has been subjected to thorough and extensive investigation. Persistent activation of Wnt signaling exerts diverse cancer characteristics, encompassing tumor initiation, tumor growth, cell senescence, cell death, differentiation, and metastasis. Here we review the principal signaling mechanisms and the regulatory influence of pathway-intrinsic and extrinsic kinases on cancer progression. Additionally, we underscore the divergences and intricate interplays of the canonical and non-canonical Wnt signaling pathways and their critical influence in cancer pathophysiology, exhibiting both growth-promoting and growth-suppressing roles across diverse cancer types. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer and Cancer Therapy)
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16 pages, 2489 KiB  
Review
Extracellular Signal-Regulated Kinases: One Pathway, Multiple Fates
by Xavier Deschênes-Simard, Mohan Malleshaiah and Gerardo Ferbeyre
Cancers 2024, 16(1), 95; https://doi.org/10.3390/cancers16010095 - 24 Dec 2023
Cited by 1 | Viewed by 3045
Abstract
This comprehensive review delves into the multifaceted aspects of ERK signaling and the intricate mechanisms underlying distinct cellular fates. ERK1 and ERK2 (ERK) govern proliferation, transformation, epithelial–mesenchymal transition, differentiation, senescence, or cell death, contingent upon activation strength, duration, and context. The biochemical mechanisms [...] Read more.
This comprehensive review delves into the multifaceted aspects of ERK signaling and the intricate mechanisms underlying distinct cellular fates. ERK1 and ERK2 (ERK) govern proliferation, transformation, epithelial–mesenchymal transition, differentiation, senescence, or cell death, contingent upon activation strength, duration, and context. The biochemical mechanisms underlying these outcomes are inadequately understood, shaped by signaling feedback and the spatial localization of ERK activation. Generally, ERK activation aligns with the Goldilocks principle in cell fate determination. Inadequate or excessive ERK activity hinders cell proliferation, while balanced activation promotes both cell proliferation and survival. Unraveling the intricacies of how the degree of ERK activation dictates cell fate requires deciphering mechanisms encompassing protein stability, transcription factors downstream of ERK, and the chromatin landscape. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer and Cancer Therapy)
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19 pages, 7011 KiB  
Review
Semaphorin 6 Family—An Important Yet Overlooked Group of Signaling Proteins Involved in Cancerogenesis
by Wiktor Wagner, Błażej Ochman and Waldemar Wagner
Cancers 2023, 15(23), 5536; https://doi.org/10.3390/cancers15235536 - 22 Nov 2023
Cited by 2 | Viewed by 2460
Abstract
According to recent evidence, some groups of semaphorins (SEMAs) have been associated with cancer progression. These proteins are able to modulate the cellular signaling of particular receptor tyrosine kinases (RTKs) via the stimulation of SEMA-specific coreceptors, namely plexins (plexin-A, -B, -C, -D) and [...] Read more.
According to recent evidence, some groups of semaphorins (SEMAs) have been associated with cancer progression. These proteins are able to modulate the cellular signaling of particular receptor tyrosine kinases (RTKs) via the stimulation of SEMA-specific coreceptors, namely plexins (plexin-A, -B, -C, -D) and neuropilins (Np1, Np2), which share common domains with RTKs, leading to the coactivation of the latter receptors. MET, ERBB2, VEGFR2, PFGFR, and EGFR, among others, represent acknowledged targets of semaphorins that are often associated with tumor progression or poor prognosis. In particular, higher expression of SEMA6 family proteins in cancer cells and stromal cells of the cancer niche is often associated with enhanced tumor angiogenesis, metastasis, and resistance to anticancer therapy. Notably, high SEMA6 expression in malignant tumor cells such as melanoma, pleural mesothelioma, gastric cancer, lung adenocarcinoma, and glioblastoma may serve as a prognostic biomarker of tumor progression. To date, very few studies have focused on the mechanisms of transmembrane SEMA6-driven tumor progression and its underlying interplay with RTKs within the tumor microenvironment. This review presents the growing evidence in the literature on the complex and shaping role of SEMA6 family proteins in cancer responsiveness to environmental stimuli. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer and Cancer Therapy)
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23 pages, 1046 KiB  
Review
Targeted Alpha Therapy (TAT) with Single-Domain Antibodies (Nanobodies)
by Kate Hurley, Meiyun Cao, Haiming Huang and Yi Wang
Cancers 2023, 15(13), 3493; https://doi.org/10.3390/cancers15133493 - 4 Jul 2023
Cited by 1 | Viewed by 3135
Abstract
The persistent threat of cancer necessitates the development of improved and more efficient therapeutic strategies that limit damage to healthy tissues. Targeted alpha therapy (TαT), a novel form of radioimmuno-therapy (RIT), utilizes a targeting vehicle, commonly antibodies, to deliver high-energy, but short-range, alpha-emitting [...] Read more.
The persistent threat of cancer necessitates the development of improved and more efficient therapeutic strategies that limit damage to healthy tissues. Targeted alpha therapy (TαT), a novel form of radioimmuno-therapy (RIT), utilizes a targeting vehicle, commonly antibodies, to deliver high-energy, but short-range, alpha-emitting particles specifically to cancer cells, thereby reducing toxicity to surrounding normal tissues. Although full-length antibodies are often employed as targeting vehicles for TαT, their high molecular weight and the presence of an Fc-region lead to a long blood half-life, increased bone marrow toxicity, and accumulation in other tissues such as the kidney, liver, and spleen. The discovery of single-domain antibodies (sdAbs), or nanobodies, naturally occurring in camelids and sharks, has introduced a novel antigen-specific vehicle for molecular imaging and TαT. Given that nanobodies are the smallest naturally occurring antigen-binding fragments, they exhibit shorter relative blood half-lives, enhanced tumor uptake, and equivalent or superior binding affinity and specificity. Nanobody technology could provide a viable solution for the off-target toxicity observed with full-length antibody-based TαT. Notably, the pharmacokinetic properties of nanobodies align better with the decay characteristics of many short-lived α-emitting radionuclides. This review aims to encapsulate recent advancements in the use of nanobodies as a vehicle for TαT. Full article
(This article belongs to the Special Issue Cell Signaling in Cancer and Cancer Therapy)
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