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Molecular Mechanisms of Tumor Suppressor Genes
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Molecular Mechanisms of Tumor Suppressor Genes

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

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 11030

Special Issue Editor

Dr. Kwang Dong Kim

E-Mail Website
Guest Editor
Division of Applied Life Science (BK21 Plus), Gyeongsang National University, Jinju 52828, Republic of Korea
Interests: autophagy; apoptosis; biofunctional natural materials; skin-whitening; tumor suppressor

Special Issue Information

Dear Colleagues,

Cancer develops through a multi-step process. Germline or somatic gene alterations and clonal selection of precancerous cells are the main driving forces in this process. Most human cancers are caused by genetic and epigenetic changes in cells, and such genetic transformations lead to uncontrolled cell proliferation, resistance to apoptosis, immortalization, activation of invasion and metastasis, immune evasion, and angiogenesis, contributing to the hallmarks of malignant cancer. Tumor suppressor genes that inhibit the development of malignancies are known to lose functions in tumor cells through loss-of-function mutation, epigenetic suppression, and miRNA-mediated suppression of expression. For example, p53 is one of the most important tumor suppressor genes frequently mutated in human cancers. Strategies targeting p53 have been developed, including gene therapy to restore p53 function, inhibition of the p53-MDM2 interaction, restoration of mutant p53 to wild-type p53, targeting of p53 family proteins, ablation of mutant p53, and p53-based vaccines. Some treatments are known to be in clinical trials. Therefore, it is expected that a series of research processes such as the discovery of more tumor suppressor genes, identification of antitumor mechanisms by gene expression, and development of therapeutics targeting the tumor suppressor genes will greatly contribute to overcoming tumors.

This Special Issue of IJMS aims to provide a comprehensive overview of the latest research on tumor suppressor genes, from molecular and cell biological mechanisms to their application as tumor therapeutic targets, with a special focus on the relationship between tumor suppressor gene expression regulation and tumorigenesis.

Dr. Kwang Dong Kim
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

  • tumor suppressor
  • genetic mutation
  • epigenetic regulation
  • clinicopathological characterization and prognosis
  • protein-protein interaction
  • signal transduction
  • cell proliferation
  • invasion/epithelial–mesenchymal transition
  • apoptosis
  • autophagy
  • anticancer drug resistance
  • gene therapy
  • metabolic stress
  • therapeutical approaches

Published Papers (4 papers)

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Research

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18 pages, 2015 KiB  
Article
Uncovering Oncogenic Mechanisms of Tumor Suppressor Genes in Breast Cancer Multi-Omics Data
by Seong Beom Cho
Int. J. Mol. Sci. 2022, 23(17), 9624; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23179624 - 25 Aug 2022
Cited by 1 | Viewed by 1737
Abstract
Tumor suppressor genes (TSGs) are essential genes in the development of cancer. While they have many roles in normal cells, mutation and dysregulation of the TSGs result in aberrant molecular processes in cancer cells. Therefore, understanding TSGs and their roles in the oncogenic [...] Read more.
Tumor suppressor genes (TSGs) are essential genes in the development of cancer. While they have many roles in normal cells, mutation and dysregulation of the TSGs result in aberrant molecular processes in cancer cells. Therefore, understanding TSGs and their roles in the oncogenic process is crucial for prevention and treatment of cancer. In this research, multi-omics breast cancer data were used to identify molecular mechanisms of TSGs in breast cancer. Differentially expressed genes and differentially coexpressed genes were identified in four large-scale transcriptomics data from public repositories and multi-omics data analyses of copy number, methylation and gene expression were performed. The results of the analyses were integrated using enrichment analysis and meta-analysis of a p-value summation method. The integrative analysis revealed that TSGs have a significant relationship with genes of gene ontology terms that are related to cell cycle, genome stability, RNA processing and metastasis, indicating the regulatory mechanisms of TSGs on cancer cells. The analysis frame and research results will provide valuable information for the further identification of TSGs in different types of cancers. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Tumor Suppressor Genes)
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20 pages, 3043 KiB  
Article
TKTL1 Knockdown Impairs Hypoxia-Induced Glucose-6-phosphate Dehydrogenase and Glyceraldehyde-3-phosphate Dehydrogenase Overexpression
by Inês Baptista, Effrosyni Karakitsou, Jean-Baptiste Cazier, Ulrich L. Günther, Silvia Marin and Marta Cascante
Int. J. Mol. Sci. 2022, 23(7), 3574; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073574 - 25 Mar 2022
Cited by 7 | Viewed by 3113
Abstract
Increased expression of transketolase (TKT) and its isoform transketolase-like-1 (TKTL1) has been related to the malignant leukemia phenotype through promoting an increase in the non-oxidative branch of the pentose phosphate pathway (PPP). Recently, it has also been described that TKTL1 can have a [...] Read more.
Increased expression of transketolase (TKT) and its isoform transketolase-like-1 (TKTL1) has been related to the malignant leukemia phenotype through promoting an increase in the non-oxidative branch of the pentose phosphate pathway (PPP). Recently, it has also been described that TKTL1 can have a role in survival under hypoxic conditions and in the acquisition of radio resistance. However, TKTL1’s role in triggering metabolic reprogramming under hypoxia in leukemia cells has never been characterized. Using THP-1 AML cells, and by combining metabolomics and transcriptomics techniques, we characterized the impact of TKTL1 knockdown on the metabolic reprogramming triggered by hypoxia. Results demonstrated that TKTL1 knockdown results in a decrease in TKT, glucose-6-phosphate dehydrogenase (G6PD) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activities and impairs the hypoxia-induced overexpression of G6PD and GAPDH, all having significant impacts on the redox capacity of NADPH- and NADH-related cells. Moreover, TKTL1 knockdown impedes hypoxia-induced transcription of genes encoding key enzymes and transporters involved in glucose, PPP and amino acid metabolism, rendering cells unable to switch to enhanced glycolysis under hypoxia. Altogether, our results show that TKTL1 plays a key role in the metabolic adaptation to hypoxia in THP-1 AML cells through modulation of G6PD and GAPDH activities, both regulating glucose/glutamine consumption and the transcriptomic overexpression of key players of PPP, glucose and amino acids metabolism. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Tumor Suppressor Genes)
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Review

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14 pages, 2626 KiB  
Review
The Function of N-Myc Downstream-Regulated Gene 2 (NDRG2) as a Negative Regulator in Tumor Cell Metastasis
by Ki Won Lee, Seyeon Lim and Kwang Dong Kim
Int. J. Mol. Sci. 2022, 23(16), 9365; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23169365 - 19 Aug 2022
Cited by 9 | Viewed by 1950
Abstract
N-myc downstream-regulated gene 2 (NDRG2) is a tumor-suppressor gene that suppresses tumorigenesis and metastasis of tumors and increases sensitivity to anti-cancer drugs. In this review, we summarize information on the clinicopathological characteristics of tumor patients according to NDRG2 expression in various tumor tissues [...] Read more.
N-myc downstream-regulated gene 2 (NDRG2) is a tumor-suppressor gene that suppresses tumorigenesis and metastasis of tumors and increases sensitivity to anti-cancer drugs. In this review, we summarize information on the clinicopathological characteristics of tumor patients according to NDRG2 expression in various tumor tissues and provide information on the metastasis inhibition-related cell signaling modulation by NDRG2. Loss of NDRG2 expression is a prognostic factor that correlates with TNM grade and tumor metastasis and has an inverse relationship with patient survival in various tumor patients. NDRG2 inhibits cell signaling, such as AKT-, NF-κB-, STAT3-, and TGF-β-mediated signaling, to induce tumor metastasis, and induces activation of GSK-3β which has anti-tumor effects. Although NDRG2 operates as an adaptor protein to mediate the interaction between kinases and phosphatases, which is essential in regulating cell signaling related to tumor metastasis, the molecular mechanism of NDRG2 as an adapter protein does not seem to be fully elucidated. This review aims to assist the research design regarding NDRG2 function as an adaptor protein and suggests NDRG2 as a molecular target to inhibit tumor metastasis and improve the prognosis in tumor patients. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Tumor Suppressor Genes)
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20 pages, 1082 KiB  
Review
The Therapeutic Potential of the Restoration of the p53 Protein Family Members in the EGFR-Mutated Lung Cancer
by Matilde Fregni, Yari Ciribilli and Joanna E. Zawacka-Pankau
Int. J. Mol. Sci. 2022, 23(13), 7213; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23137213 - 29 Jun 2022
Cited by 2 | Viewed by 3527
Abstract
Despite the recent development of precision medicine and targeted therapies, lung cancer remains the top cause of cancer-related mortality worldwide. The patients diagnosed with metastatic disease have a five-year survival rate lower than 6%. In metastatic disease, EGFR is the most common driver [...] Read more.
Despite the recent development of precision medicine and targeted therapies, lung cancer remains the top cause of cancer-related mortality worldwide. The patients diagnosed with metastatic disease have a five-year survival rate lower than 6%. In metastatic disease, EGFR is the most common driver of mutation, with the most common co-driver hitting TP53. EGFR-positive patients are offered the frontline treatment with tyrosine kinase inhibitors, yet the development of resistance and the lack of alternative therapies make this group of patients only fit for clinical trial participation. Since mutant p53 is the most common co-driver in the metastatic setting, therapies reactivating the p53 pathway might serve as a promising alternative therapeutic approach in patients who have developed a resistance to tyrosine kinase inhibitors. This review focuses on the molecular background of EGFR-mutated lung cancer and discusses novel therapeutic options converging on the reactivation of p53 tumor suppressor pathways. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Tumor Suppressor Genes)
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