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Cancers
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Unique Perspectives in Cancer Signaling
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Unique Perspectives in Cancer Signaling

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (15 September 2024) | Viewed by 17045

Special Issue Editor

Dr. Peiwen Fei

E-Mail Website
Guest Editor
1. Cancer Biology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA
2. Graduate Program of Molecular Biosciences and Bioengineering, University of Hawaii, Honolulu, HI 96813, USA
Interests: cancer signaling; cancer etiology; Fanconi anemia (FA) signaling; cancer treatment; genetic model; cancer genetics and biology

Special Issue Information

Dear Colleagues, 

We are pleased to introduce a Special Issue on cancer signaling with a focus on unique, interdisciplinary perspectives for investigating key pathways that drive cancer initiation and progression. These perspectives can entail novel technological–computational implementations, translational–clinical-level applications, or even epidemiological enhancements of basic science understandings. Across these diverse inquiries, this edition on “Cancer Signaling” aims to define nuanced contexts surrounding oncogenic signaling for the development of therapeutic and preventive strategies against various cancers. Reviews are expected to focus on specific disease types or signaling pathways through a multidisciplinary lens. Original research articles with a focus along these scopes will also be considered.

Dr. Peiwen Fei
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 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

  • oncogenesis
  • cancer signaling
  • technology
  • translational
  • clinical
  • epidemiology

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Published Papers (7 papers)

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Research

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20 pages, 5831 KiB  
Article
Effects of KEAP1 Silencing on NRF2 and NOTCH Pathways in SCLC Cell Lines
by Federico Pio Fabrizio, Angelo Sparaneo, Giusy Gorgoglione, Pierpaolo Battista, Flavia Centra, Francesco Delli Muti, Domenico Trombetta, Antonella Centonza, Paolo Graziano, Antonio Rossi, Vito Michele Fazio and Lucia Anna Muscarella
Cancers 2024, 16(10), 1885; https://doi.org/10.3390/cancers16101885 - 15 May 2024
Viewed by 1339
Abstract
The KEAP1/NRF2 pathway is a master regulator of several redox-sensitive genes implicated in the resistance of tumor cells against therapeutic drugs. The dysfunction of the KEAP1/NRF2 system has been correlated with neoplastic patients’ outcomes and responses to conventional therapies. In lung tumors, the [...] Read more.
The KEAP1/NRF2 pathway is a master regulator of several redox-sensitive genes implicated in the resistance of tumor cells against therapeutic drugs. The dysfunction of the KEAP1/NRF2 system has been correlated with neoplastic patients’ outcomes and responses to conventional therapies. In lung tumors, the growth and the progression of cancer cells may also involve the intersection between the molecular NRF2/KEAP1 axis and other pathways, including NOTCH, with implications for antioxidant protection, survival of cancer cells, and drug resistance to therapies. At present, the data concerning the mechanism of aberrant NRF2/NOTCH crosstalk as well as its genetic and epigenetic basis in SCLC are incomplete. To better clarify this point and elucidate the contribution of NRF2/NOTCH crosstalk deregulation in tumorigenesis of SCLC, we investigated genetic and epigenetic dysfunctions of the KEAP1 gene in a subset of SCLC cell lines. Moreover, we assessed its impact on SCLC cells’ response to conventional chemotherapies (etoposide, cisplatin, and their combination) and NOTCH inhibitor treatments using DAPT, a γ-secretase inhibitor (GSI). We demonstrated that the KEAP1/NRF2 axis is epigenetically controlled in SCLC cell lines and that silencing of KEAP1 by siRNA induced the upregulation of NRF2 with a consequent increase in SCLC cells’ chemoresistance under cisplatin and etoposide treatment. Moreover, KEAP1 modulation also interfered with NOTCH1, HES1, and DLL3 transcription. Our preliminary data provide new insights about the downstream effects of KEAP1 dysfunction on NRF2 and NOTCH deregulation in this type of tumor and corroborate the hypothesis of a cooperation of these two pathways in the tumorigenesis of SCLC. Full article
(This article belongs to the Special Issue Unique Perspectives in Cancer Signaling)
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11 pages, 2300 KiB  
Article
The Impact of Digital Inequities on Esophageal Cancer Disparities in the US
by David J. Fei-Zhang, Evan R. Edwards, Shravan Asthana, Daniel C. Chelius, Anthony M. Sheyn and Jeffrey C. Rastatter
Cancers 2023, 15(23), 5522; https://doi.org/10.3390/cancers15235522 - 22 Nov 2023
Cited by 2 | Viewed by 1093
Abstract
Background: There is currently no comprehensive tool that quantifiably measures validated factors of modern technology access in the US for digital inequity impact on esophageal cancer care (EC). Objective: To assess the influence of digital inequities on esophageal cancer disparities while accounting for [...] Read more.
Background: There is currently no comprehensive tool that quantifiably measures validated factors of modern technology access in the US for digital inequity impact on esophageal cancer care (EC). Objective: To assess the influence of digital inequities on esophageal cancer disparities while accounting for traditional social determinants. Methods: 15,656 EC patients from 2013–2017 in SEER were assessed for significant regression trends in long-term follow-up, survival, prognosis, and treatment with increasing overall digital inequity, as measured by the Digital Inequity Index (DII). The DII was calculated based on 17 census tract-level variables derived from the American Community Survey and Federal Communications Commission. Variables were categorized as infrastructure access or sociodemographic, ranked, and then averaged into a composite score. Results: With increasing overall digital inequity, significant decreases in the length of long-term follow-up (p < 0.001) and survival (p < 0.001) for EC patients were observed. EC patients showed decreased odds of receiving indicated surgical resection (OR 0.97, 95% CI 0.95–99) with increasing digital inequity. They also showed increased odds of advanced preliminary staging (OR 1.02, 95% CI 1.00–1.05) and decreased odds of receiving indicated chemotherapy (OR 0.97;95% CI 0.95–99). Conclusions: Digital inequities meaningfully contribute to detrimental trends in EC patient care in the US, allowing discourse for targeted means of alleviating disparities while contextualizing national, sociodemographic trends of the impact of online access on informed care. Full article
(This article belongs to the Special Issue Unique Perspectives in Cancer Signaling)
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Review

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23 pages, 715 KiB  
Review
Dissecting the Puzzling Roles of FAM46C: A Multifaceted Pan-Cancer Tumour Suppressor with Increasing Clinical Relevance
by Giancarlo Lai, Federica De Grossi, Ilaria Catusi, Elisa Pesce and Nicola Manfrini
Cancers 2024, 16(9), 1706; https://doi.org/10.3390/cancers16091706 - 27 Apr 2024
Cited by 2 | Viewed by 1489
Abstract
FAM46C is a well-established tumour suppressor with a role that is not completely defined or universally accepted. Although FAM46C expression is down-modulated in several tumours, significant mutations in the FAM46C gene are only found in multiple myeloma (MM). Consequently, its tumour suppressor activity [...] Read more.
FAM46C is a well-established tumour suppressor with a role that is not completely defined or universally accepted. Although FAM46C expression is down-modulated in several tumours, significant mutations in the FAM46C gene are only found in multiple myeloma (MM). Consequently, its tumour suppressor activity has primarily been studied in the MM context. However, emerging evidence suggests that FAM46C is involved also in other cancer types, namely colorectal, prostate and gastric cancer and squamous cell and hepatocellular carcinoma, where FAM46C expression was found to be significantly reduced in tumoural versus non-tumoural tissues and where FAM46C was shown to possess anti-proliferative properties. Accordingly, FAM46C was recently proposed to function as a pan-cancer prognostic marker, bringing FAM46C under the spotlight and attracting growing interest from the scientific community in the pathways modulated by FAM46C and in its mechanistic activity. Here, we will provide the first comprehensive review regarding FAM46C by covering (1) the intracellular pathways regulated by FAM46C, namely the MAPK/ERK, PI3K/AKT, β-catenin and TGF-β/SMAD pathways; (2) the models regarding its mode of action, specifically the poly(A) polymerase, intracellular trafficking modulator and inhibitor of centriole duplication models, focusing on connections and interdependencies; (3) the regulation of FAM46C expression in different environments by interferons, IL-4, TLR engagement or transcriptional modulators; and, lastly, (4) how FAM46C expression levels associate with increased/decreased tumour cell sensitivity to anticancer agents, such as bortezomib, dexamethasone, lenalidomide, pomalidomide, doxorubicin, melphalan, SK1-I, docetaxel and norcantharidin. Full article
(This article belongs to the Special Issue Unique Perspectives in Cancer Signaling)
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29 pages, 2961 KiB  
Review
Krüppel-like Factor-9 and Krüppel-like Factor-13: Highly Related, Multi-Functional, Transcriptional Repressors and Activators of Oncogenesis
by Frank A. Simmen, Iad Alhallak and Rosalia C. M. Simmen
Cancers 2023, 15(23), 5667; https://doi.org/10.3390/cancers15235667 - 30 Nov 2023
Cited by 2 | Viewed by 1741
Abstract
Specificity Proteins/Krüppel-like Factors (SP/KLF family) are a conserved family of transcriptional regulators. These proteins share three highly conserved, contiguous zinc fingers in their carboxy-terminus, requisite for binding to cis elements in DNA. Each SP/KLF protein has unique primary sequence within its amino-terminal and [...] Read more.
Specificity Proteins/Krüppel-like Factors (SP/KLF family) are a conserved family of transcriptional regulators. These proteins share three highly conserved, contiguous zinc fingers in their carboxy-terminus, requisite for binding to cis elements in DNA. Each SP/KLF protein has unique primary sequence within its amino-terminal and carboxy-terminal regions, and it is these regions which interact with co-activators, co-repressors, and chromatin-modifying proteins to support the transcriptional activation and repression of target genes. Krüppel-like Factor 9 (KLF9) and Krüppel-like Factor 13 (KLF13) are two of the smallest members of the SP/KLF family, are paralogous, emerged early in metazoan evolution, and are highly conserved. Paradoxically, while most similar in primary sequence, KLF9 and KLF13 display many distinct roles in target cells. In this article, we summarize the work that has identified the roles of KLF9 (and to a lesser degree KLF13) in tumor suppression or promotion via unique effects on differentiation, pro- and anti-inflammatory pathways, oxidative stress, and tumor immune cell infiltration. We also highlight the great diversity of miRNAs, lncRNAs, and circular RNAs which provide mechanisms for the ubiquitous tumor-specific suppression of KLF9 mRNA and protein. Elucidation of KLF9 and KLF13 in cancer biology is likely to provide new inroads to the understanding of oncogenesis and its prevention and treatments. Full article
(This article belongs to the Special Issue Unique Perspectives in Cancer Signaling)
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18 pages, 2142 KiB  
Review
The Role of TRAIL in Apoptosis and Immunosurveillance in Cancer
by Julio M. Pimentel, Jun-Ying Zhou and Gen Sheng Wu
Cancers 2023, 15(10), 2752; https://doi.org/10.3390/cancers15102752 - 13 May 2023
Cited by 30 | Viewed by 4634
Abstract
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily that selectively induces apoptosis in tumor cells without harming normal cells, making it an attractive agent for cancer therapy. TRAIL induces apoptosis by binding to and activating its death [...] Read more.
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily that selectively induces apoptosis in tumor cells without harming normal cells, making it an attractive agent for cancer therapy. TRAIL induces apoptosis by binding to and activating its death receptors DR4 and DR5. Several TRAIL-based treatments have been developed, including recombinant forms of TRAIL and its death receptor agonist antibodies, but the efficacy of TRAIL-based therapies in clinical trials is modest. In addition to inducing cancer cell apoptosis, TRAIL is expressed in immune cells and plays a critical role in tumor surveillance. Emerging evidence indicates that the TRAIL pathway may interact with immune checkpoint proteins, including programmed death-ligand 1 (PD-L1), to modulate PD-L1-based tumor immunotherapies. Therefore, understanding the interaction between TRAIL and the immune checkpoint PD-L1 will lead to the development of new strategies to improve TRAIL- and PD-L1-based therapies. This review discusses recent findings on TRAIL-based therapy, resistance, and its involvement in tumor immunosurveillance. Full article
(This article belongs to the Special Issue Unique Perspectives in Cancer Signaling)
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19 pages, 1752 KiB  
Review
Deepening Our Understanding of the Factors Affecting Landscape of Myeloproliferative Neoplasms: What Do We Know about Them?
by María Luz Morales and Francisca Ferrer-Marín
Cancers 2023, 15(4), 1348; https://doi.org/10.3390/cancers15041348 - 20 Feb 2023
Cited by 4 | Viewed by 2397
Abstract
Myeloproliferative neoplasms (MPNs) arise from the uncontrolled proliferation of hematopoietic stem and progenitor cells in bone marrow. As with all tumors, the development of MPNs is a consequence of alterations in malignant cells and their interaction with other extrinsic factors that support and [...] Read more.
Myeloproliferative neoplasms (MPNs) arise from the uncontrolled proliferation of hematopoietic stem and progenitor cells in bone marrow. As with all tumors, the development of MPNs is a consequence of alterations in malignant cells and their interaction with other extrinsic factors that support and promote tumor progression. Since the discovery of driver mutations, much work has focused on studying and reviewing the genomic features of the disease but has neglected to delve into the important role that many other mechanisms may play. This review discusses the genetic component of MPNs but focuses mainly on some of the most relevant work investigating other non-genetic factors that may be crucial for the disease. The studies summarized here address MPN cell-intrinsic or -extrinsic factors and the interaction between them through transcriptomic, proteomic and microbiota studies, among others. Full article
(This article belongs to the Special Issue Unique Perspectives in Cancer Signaling)
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23 pages, 919 KiB  
Review
Potential Pathophysiological Pathways in the Complex Relationships between OSA and Cancer
by Manuel Sánchez-de-la-Torre, Carolina Cubillos, Olivia J. Veatch, Francisco Garcia-Rio, David Gozal and Miguel Angel Martinez-Garcia
Cancers 2023, 15(4), 1061; https://doi.org/10.3390/cancers15041061 - 7 Feb 2023
Cited by 16 | Viewed by 3561
Abstract
Several epidemiological and clinical studies have suggested a relationship between obstructive sleep apnea (OSA) and a higher incidence or severity of cancer. This relationship appears to be dependent on a myriad of factors. These include non-modifiable factors, such as age and gender; and [...] Read more.
Several epidemiological and clinical studies have suggested a relationship between obstructive sleep apnea (OSA) and a higher incidence or severity of cancer. This relationship appears to be dependent on a myriad of factors. These include non-modifiable factors, such as age and gender; and modifiable or preventable factors, such as specific comorbidities (especially obesity), the use of particular treatments, and, above all, the histological type or location of the cancer. Heterogeneity in the relationship between OSA and cancer is also related to the influences of intermittent hypoxemia (a hallmark feature of OSA), among others, on metabolism and the microenvironment of different types of tumoral cells. The hypoxia inducible transcription factor (HIF-1α), a molecule activated and expressed in situations of hypoxemia, seems to be key to enabling a variety of pathophysiological mechanisms that are becoming increasingly better recognized. These mechanisms appear to be operationally involved via alterations in different cellular functions (mainly involving the immune system) and molecular functions, and by inducing modifications in the microbiome. This, in turn, may individually or collectively increase the risk of cancer, which is then, further modulated by the genetic susceptibility of the individual. Here, we provide an updated and brief review of the different pathophysiological pathways that have been identified and could explain the relationship between OSA and cancer. We also identify future challenges that need to be overcome in this intriguing field of research. Full article
(This article belongs to the Special Issue Unique Perspectives in Cancer Signaling)
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