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Cancers
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Recent Advances in Tumor Suppressor
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Recent Advances in Tumor Suppressor

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

Deadline for manuscript submissions: closed (1 December 2023) | Viewed by 22431

Special Issue Editor

Prof. Dr. Chiaki Takahashi

E-Mail Website
Guest Editor
Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University, Ishikawa 920-1192, Japan
Interests: oncogene; tumor suppressor; tumor metabolism; RB; Ras; RECK
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The era of investigations on tumor suppressor genes was initiated by the discovery of retinoblastoma tumor suppressor 1 gene (RB1) and Trp53 tumor suppressor gene that took place more than three decades ago. RB1 primarily regulates G1/S transition during cell cycle progression by modulating the activity of E2F transcription factors. RB mutation was initially discovered by virtue of its role in tumor initiation.

However, it is becoming clear that, in the majority of cancers, somatic RB1 inactivation occurs rather during tumor progression. The consequence of RB1 inactivation in this context contains epithelial mesenchymal transition (EMT), invasion, metastasis, undifferentiated status, tumor microenvironment, therapy resistance, etc.

As is in case of RB1, recent studies uncovered numerous novel functions in tumor suppressors that were unexpected in early studies. The aim of this Special Issue of Cancers is to highlight studies focusing on previously unexpected functions of various tumor suppressors including RB1. We welcome submissions that will contribute to deepen our understanding of cancers from the view of the complicated functions of tumor suppressors.

Prof. Dr. Chiaki Takahashi
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

  • retinoblastoma
  • RB
  • E2F
  • cell cycle
  • cancer progression

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Published Papers (5 papers)

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Research

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27 pages, 8394 KiB  
Article
WWOX Loses the Ability to Regulate Oncogenic AP-2γ and Synergizes with Tumor Suppressor AP-2α in High-Grade Bladder Cancer
by Damian Kołat, Żaneta Kałuzińska, Andrzej K. Bednarek and Elżbieta Płuciennik
Cancers 2021, 13(12), 2957; https://doi.org/10.3390/cancers13122957 - 12 Jun 2021
Cited by 7 | Viewed by 3126
Abstract
The cytogenic locus of the WWOX gene overlaps with the second most active fragile site, FRA16D, which is present at a higher frequency in bladder cancer (BLCA) patients with smoking habit, a known risk factor of this tumor. Recently, we demonstrated the relevance [...] Read more.
The cytogenic locus of the WWOX gene overlaps with the second most active fragile site, FRA16D, which is present at a higher frequency in bladder cancer (BLCA) patients with smoking habit, a known risk factor of this tumor. Recently, we demonstrated the relevance of the role of WWOX in grade 2 BLCA in collaboration with two AP-2 transcription factors whose molecular actions supported or opposed pro-cancerous events, suggesting a distinct character. As further research is needed on higher grades, the aim of the present study was to examine WWOX-AP-2 functionality in grade 3 and 4 BLCA using equivalent in vitro methodology with additional transcriptome profiling of cellular variants. WWOX and AP-2α demonstrated similar anti-cancer functionality in most biological processes with subtle differences in MMP-2/9 regulation; this contradicted that of AP-2γ, whose actions potentiated cancer progression. Simultaneous overexpression of WWOX and AP-2α/AP-2γ revealed that single discrepancies appear in WWOX-AP-2α collaboration but only at the highest BLCA grade; WWOX-AP-2α collaboration was considered anti-cancer. However, WWOX only appeared to have residual activity against oncogenic AP-2γ in grade 3 and 4: variants with either AP-2γ overexpression alone or combined WWOX and AP-2γ overexpression demonstrated similar pro-tumoral behavior. Transcriptome profiling with further gene ontology certified biological processes investigated in vitro and indicated groups of genes consisting of AP-2 targets and molecules worth investigation as biomarkers. In conclusion, tumor suppressor synergism between WWOX and AP-2α is unimpaired in high-grade BLCA compared to intermediate grade, yet the ability of WWOX to guide oncogenic AP-2γ is almost completely lost. Full article
(This article belongs to the Special Issue Recent Advances in Tumor Suppressor)
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17 pages, 4291 KiB  
Article
Loss of Rb1 Enhances Glycolytic Metabolism in Kras-Driven Lung Tumors In Vivo
by Lindsey R. Conroy, Susan Dougherty, Traci Kruer, Stephanie Metcalf, Pawel Lorkiewicz, Liqing He, Xinmin Yin, Xiang Zhang, Sengodagounder Arumugam, Lyndsay E.A. Young, Ramon C. Sun and Brian F. Clem
Cancers 2020, 12(1), 237; https://doi.org/10.3390/cancers12010237 - 17 Jan 2020
Cited by 13 | Viewed by 4477
Abstract
Dysregulated metabolism is a hallmark of cancer cells and is driven in part by specific genetic alterations in various oncogenes or tumor suppressors. The retinoblastoma protein (pRb) is a tumor suppressor that canonically regulates cell cycle progression; however, recent studies have highlighted a [...] Read more.
Dysregulated metabolism is a hallmark of cancer cells and is driven in part by specific genetic alterations in various oncogenes or tumor suppressors. The retinoblastoma protein (pRb) is a tumor suppressor that canonically regulates cell cycle progression; however, recent studies have highlighted a functional role for pRb in controlling cellular metabolism. Here, we report that loss of the gene encoding pRb (Rb1) in a transgenic mutant Kras-driven model of lung cancer results in metabolic reprogramming. Our tracer studies using bolus dosing of [U-13C]-glucose revealed an increase in glucose carbon incorporation into select glycolytic intermediates. Consistent with this result, Rb1-depleted tumors exhibited increased expression of key glycolytic enzymes. Interestingly, loss of Rb1 did not alter mitochondrial pyruvate oxidation compared to lung tumors with intact Rb1. Additional tracer studies using [U-13C,15N]-glutamine and [U-13C]-lactate demonstrated that loss of Rb1 did not alter glutaminolysis or utilization of circulating lactate within the tricarboxylic acid cycle (TCA) in vivo. Taken together, these data suggest that the loss of Rb1 promotes a glycolytic phenotype, while not altering pyruvate oxidative metabolism or glutamine anaplerosis in Kras-driven lung tumors. Full article
(This article belongs to the Special Issue Recent Advances in Tumor Suppressor)
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Review

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18 pages, 12503 KiB  
Review
Tumor Suppressor Candidate 2 (TUSC2): Discovery, Functions, and Cancer Therapy
by Austin Arrigo, Angelina T. Regua, Mariana K. Najjar and Hui-Wen Lo
Cancers 2023, 15(9), 2455; https://doi.org/10.3390/cancers15092455 - 25 Apr 2023
Cited by 2 | Viewed by 2241
Abstract
Tumor Suppressor Candidate 2 (TUSC2) was first discovered as a potential tumor suppressor gene residing in the frequently deleted 3p21.3 chromosomal region. Since its discovery, TUSC2 has been found to play vital roles in normal immune function, and TUSC2 loss is associated with [...] Read more.
Tumor Suppressor Candidate 2 (TUSC2) was first discovered as a potential tumor suppressor gene residing in the frequently deleted 3p21.3 chromosomal region. Since its discovery, TUSC2 has been found to play vital roles in normal immune function, and TUSC2 loss is associated with the development of autoimmune diseases as well as impaired responses within the innate immune system. TUSC2 also plays a vital role in regulating normal cellular mitochondrial calcium movement and homeostasis. Moreover, TUSC2 serves as an important factor in premature aging. In addition to TUSC2′s normal cellular functions, TUSC2 has been studied as a tumor suppressor gene that is frequently deleted or lost in a multitude of cancers, including glioma, sarcoma, and cancers of the lung, breast, ovaries, and thyroid. TUSC2 is frequently lost in cancer due to somatic deletion within the 3p21.3 region, transcriptional inactivation via TUSC2 promoter methylation, post-transcriptional regulation via microRNAs, and post-translational regulation via polyubiquitination and proteasomal degradation. Additionally, restoration of TUSC2 expression promotes tumor suppression, eventuating in decreased cell proliferation, stemness, and tumor growth, as well as increased apoptosis. Consequently, TUSC2 gene therapy has been tested in patients with non-small cell lung cancer. This review will focus on the current understanding of TUSC2 functions in both normal and cancerous tissues, mechanisms of TUSC2 loss, TUSC2 cancer therapeutics, open questions, and future directions. Full article
(This article belongs to the Special Issue Recent Advances in Tumor Suppressor)
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19 pages, 1845 KiB  
Review
SMARCB1-Deficient Cancers: Novel Molecular Insights and Therapeutic Vulnerabilities
by Garrett W. Cooper and Andrew L. Hong
Cancers 2022, 14(15), 3645; https://doi.org/10.3390/cancers14153645 - 27 Jul 2022
Cited by 29 | Viewed by 8521
Abstract
SMARCB1 is a critical component of the BAF complex that is responsible for global chromatin remodeling. Loss of SMARCB1 has been implicated in the initiation of cancers such as malignant rhabdoid tumor (MRT), atypical teratoid rhabdoid tumor (ATRT), and, more recently, renal medullary [...] Read more.
SMARCB1 is a critical component of the BAF complex that is responsible for global chromatin remodeling. Loss of SMARCB1 has been implicated in the initiation of cancers such as malignant rhabdoid tumor (MRT), atypical teratoid rhabdoid tumor (ATRT), and, more recently, renal medullary carcinoma (RMC). These SMARCB1-deficient tumors have remarkably stable genomes, offering unique insights into the epigenetic mechanisms in cancer biology. Given the lack of druggable targets and the high mortality associated with SMARCB1-deficient tumors, a significant research effort has been directed toward understanding the mechanisms of tumor transformation and proliferation. Accumulating evidence suggests that tumorigenicity arises from aberrant enhancer and promoter regulation followed by dysfunctional transcriptional control. In this review, we outline key mechanisms by which loss of SMARCB1 may lead to tumor formation and cover how these mechanisms have been used for the design of targeted therapy. Full article
(This article belongs to the Special Issue Recent Advances in Tumor Suppressor)
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19 pages, 2592 KiB  
Review
The E3 Ubiquitin Ligase Fbxo4 Functions as a Tumor Suppressor: Its Biological Importance and Therapeutic Perspectives
by Shuo Qie
Cancers 2022, 14(9), 2133; https://doi.org/10.3390/cancers14092133 - 25 Apr 2022
Cited by 7 | Viewed by 2919
Abstract
Fbxo4, also known as Fbx4, belongs to the F-box protein family with a conserved F-box domain. Fbxo4 can form a complex with S-phase kinase-associated protein 1 and Cullin1 to perform its biological functions. Several proteins are identified as Fbxo4 substrates, including cyclin D1, [...] Read more.
Fbxo4, also known as Fbx4, belongs to the F-box protein family with a conserved F-box domain. Fbxo4 can form a complex with S-phase kinase-associated protein 1 and Cullin1 to perform its biological functions. Several proteins are identified as Fbxo4 substrates, including cyclin D1, Trf1/Pin2, p53, Fxr1, Mcl-1, ICAM-1, and PPARγ. Those factors can regulate cell cycle progression, cell proliferation, survival/apoptosis, and migration/invasion, highlighting their oncogenic or oncogene-like activities. Therefore, Fbxo4 is defined as a tumor suppressor. The biological functions of Fbxo4 make it a potential candidate for developing new targeted therapies. This review summarizes the gene and protein structure of Fbxo4, the mechanisms of how its expression and activity are regulated, and its substrates, biological functions, and clinicopathological importance in human cancers. Full article
(This article belongs to the Special Issue Recent Advances in Tumor Suppressor)
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