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Molecular Genetics and Epigenetics of Tumors
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Molecular Genetics and Epigenetics of Tumors

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

Deadline for manuscript submissions: closed (15 December 2022) | Viewed by 12246

Special Issue Editors

Dr. Rasika Samarasinghe

E-Mail Website
Guest Editor
School of Medicine, Deakin University, Geelong, VIC 3216, Australia
Interests: neurooncology; pediatrics; cancer biology; epigenetic; drug delivery and targeting
Dr. Amardeep Dhillon

E-Mail Website
Guest Editor
School of Medicine, Deakin University, Geelong, VIC 3216, Australia
Interests: cancer; gene regulation; signal transduction
Dr. Faiza Basheer

E-Mail Website
Guest Editor
School of Medicine, Deakin University, Geelong, VIC 3216, Australia
Interests: cancer; epigenetics; oncogenesis research

Special Issue Information

Dear Colleagues,

Alterations in the epigenetic and molecular mechanisms of tumors have proven to be critical in the development of novel and innovative diagnostics and therapies for both adult and childhood cancers. Solid tumors and hematopoietic cancers frequently harbor recurrent and specific epigenetic and molecular abnormalities such as chromosomal translocations, DNA methylation, histone modifications, long noncoding RNAs and numerous genetic mutations. Epigenetics and Molecular Genetics of Tumors, a new Special Issue, provides a thorough discussion and overview of current developments in translational research, with special emphasis on novel advances in genetics and epigenetics that can be used for clinical diagnosis, prognosis and treatment monitoring. This Special Issue will therefore bring together reviews and original articles focusing on both basic and translational research in the field of genetics and epigenetics of adult and childhood tumors.

Dr. Rasika Samarasinghe
Dr. Amardeep Dhillon
Dr. Faiza Basheer
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.

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Keywords

  • epigenetics
  • genetics
  • cancer
  • epi-markers
  • biomarkers
  • drug targets
  • drug therapy
  • DNA methylation
  • histone modification
  • chromatin
  • RNA non-coding
  • translational research

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Published Papers (4 papers)

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Research

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22 pages, 5255 KiB  
Article
Consistent DNA Hypomethylations in Prostate Cancer
by Marcos J. Araúzo-Bravo, Lars Erichsen, Pauline Ott, Agnes Beermann, Jamal Sheikh, Daniela Gerovska, Chantelle Thimm, Marcelo L. Bendhack and Simeon Santourlidis
Int. J. Mol. Sci. 2023, 24(1), 386; https://doi.org/10.3390/ijms24010386 - 26 Dec 2022
Cited by 5 | Viewed by 2633
Abstract
With approximately 1.4 million men annually diagnosed with prostate cancer (PCa) worldwide, PCa remains a dreaded threat to life and source of devastating morbidity. In recent decades, a significant decrease in age-specific PCa mortality has been achieved by increasing prostate-specific antigen (PSA) screening [...] Read more.
With approximately 1.4 million men annually diagnosed with prostate cancer (PCa) worldwide, PCa remains a dreaded threat to life and source of devastating morbidity. In recent decades, a significant decrease in age-specific PCa mortality has been achieved by increasing prostate-specific antigen (PSA) screening and improving treatments. Nevertheless, upcoming, augmented recommendations against PSA screening underline an escalating disproportion between the benefit and harm of current diagnosis/prognosis and application of radical treatment standards. Undoubtedly, new potent diagnostic and prognostic tools are urgently needed to alleviate this tensed situation. They should allow a more reliable early assessment of the upcoming threat, in order to enable applying timely adjusted and personalized therapy and monitoring. Here, we present a basic study on an epigenetic screening approach by Methylated DNA Immunoprecipitation (MeDIP). We identified genes associated with hypomethylated CpG islands in three PCa sample cohorts. By adjusting our computational biology analyses to focus on single CpG-enriched 60-nucleotide-long DNA probes, we revealed numerous consistently differential methylated DNA segments in PCa. They were associated among other genes with NOTCH3, CDK2AP1, KLK4, and ADAM15. These can be used for early discrimination, and might contribute to a new epigenetic tumor classification system of PCa. Our analysis shows that we can dissect short, differential methylated CpG-rich DNA fragments and combinations of them that are consistently present in all tumors. We name them tumor cell-specific differential methylated CpG dinucleotide signatures (TUMS). Full article
(This article belongs to the Special Issue Molecular Genetics and Epigenetics of Tumors)
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17 pages, 2662 KiB  
Article
Identification and Validation of Ferroptosis-Related DNA Methylation Signature for Predicting the Prognosis and Guiding the Treatment in Cutaneous Melanoma
by Wenna Guo, Xue Wang, Yanna Wang, Shuting Zhu, Rui Zhu and Liucun Zhu
Int. J. Mol. Sci. 2022, 23(24), 15677; https://doi.org/10.3390/ijms232415677 - 10 Dec 2022
Cited by 3 | Viewed by 2155
Abstract
Cutaneous melanoma (CM) is one of the most aggressive skin tumors with a poor prognosis. Ferroptosis is a newly discovered form of regulated cell death that is closely associated with cancer development and immunotherapy. The aim of this study was to establish and [...] Read more.
Cutaneous melanoma (CM) is one of the most aggressive skin tumors with a poor prognosis. Ferroptosis is a newly discovered form of regulated cell death that is closely associated with cancer development and immunotherapy. The aim of this study was to establish and validate a ferroptosis-related gene (FRG) DNA methylation signature to predict the prognosis of CM patients using data from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) database. A reliable four-FRG DNA methylation prognostic signature was constructed via Cox regression analysis based on TCGA database. Kaplan–Meier analysis showed that patients in the high-risk group tended to have a shorter overall survival (OS) than the low-risk group in both training TCGA and validation GEO cohorts. Time-dependent receiver operating characteristic (ROC) analysis showed the areas under the curve (AUC) at 1, 3, and 5 years were 0.738, 0.730, and 0.770 in TCGA cohort and 0.773, 0.775, and 0.905 in the validation cohort, respectively. Univariate and multivariate Cox regression analyses indicated that the signature was an independent prognostic indicator of OS in patients with CM. Immunogenomic profiling showed the low-risk group of patients had a higher immunophenoscore, and most immune checkpoints were negatively associated with the risk signature. Functional enrichment analysis revealed that immune response and immune-related pathways were enriched in the low-risk group. In conclusion, we established and validated a four-FRG DNA methylation signature that independently predicts prognosis in CM patients. This signature was strongly correlated with the immune landscape, and may serve as a biomarker to guide clinicians in making more precise and personalized treatment decisions for CM patients. Full article
(This article belongs to the Special Issue Molecular Genetics and Epigenetics of Tumors)
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20 pages, 5959 KiB  
Article
SRSF3 and HNRNPH1 Regulate Radiation-Induced Alternative Splicing of Protein Arginine Methyltransferase 5 in Hepatocellular Carcinoma
by Chaowei Wen, Zhujun Tian, Lan Li, Tongke Chen, Huajian Chen, Jichen Dai, Zhenzhen Liang, Shumei Ma and Xiaodong Liu
Int. J. Mol. Sci. 2022, 23(23), 14832; https://doi.org/10.3390/ijms232314832 - 27 Nov 2022
Cited by 8 | Viewed by 2240
Abstract
Protein arginine methyltransferase 5 (PRMT5) is an epigenetic regulator which has been proven to be a potential target for cancer therapy. We observed that PRMT5 underwent alternative splicing (AS) and generated a spliced isoform PRMT5-ISO5 in hepatocellular carcinoma (HCC) patients after radiotherapy. However, [...] Read more.
Protein arginine methyltransferase 5 (PRMT5) is an epigenetic regulator which has been proven to be a potential target for cancer therapy. We observed that PRMT5 underwent alternative splicing (AS) and generated a spliced isoform PRMT5-ISO5 in hepatocellular carcinoma (HCC) patients after radiotherapy. However, the regulatory mechanism and the clinical implications of IR-induced PRMT5 AS are unclear. This work revealed that serine and arginine rich splicing factor 3 (SRSF3) silencing increased PRMT5-ISO5 level, whereas heterogeneous nuclear ribonucleoprotein H 1 (HNRNPH1) silencing reduced it. Then, we found that SRSF3 and HNRNPH1 competitively combined with PRMT5 pre-mRNA located at the region around the 3′- splicing site on intron 2 and the alternative 3′- splicing site on exon 4. IR-induced SRSF3 downregulation led to an elevated level of PRMT5-ISO5, and exogenous expression of PRMT5-ISO5 enhanced cell radiosensitivity. Finally, we confirmed in vivo that IR induced the increased level of PRMT5-ISO5 which in turn enhanced tumor killing and regression, and liver-specific Prmt5 depletion reduced hepatic steatosis and delayed tumor progression of spontaneous HCC. In conclusion, our data uncover the competitive antagonistic interaction of SRSF3 and HNRNPH1 in regulating PRMT5 splicing induced by IR, providing potentially effective radiotherapy by modulating PRMT5 splicing against HCC. Full article
(This article belongs to the Special Issue Molecular Genetics and Epigenetics of Tumors)
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Review

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28 pages, 2043 KiB  
Review
Zebrafish Models of Paediatric Brain Tumours
by Faiza Basheer, Poshmaal Dhar and Rasika M. Samarasinghe
Int. J. Mol. Sci. 2022, 23(17), 9920; https://doi.org/10.3390/ijms23179920 - 31 Aug 2022
Cited by 2 | Viewed by 4511
Abstract
Paediatric brain cancer is the second most common childhood cancer and is the leading cause of cancer-related deaths in children. Despite significant advancements in the treatment modalities and improvements in the 5-year survival rate, it leaves long-term therapy-associated side effects in paediatric patients. [...] Read more.
Paediatric brain cancer is the second most common childhood cancer and is the leading cause of cancer-related deaths in children. Despite significant advancements in the treatment modalities and improvements in the 5-year survival rate, it leaves long-term therapy-associated side effects in paediatric patients. Addressing these impairments demands further understanding of the molecularity and heterogeneity of these brain tumours, which can be demonstrated using different animal models of paediatric brain cancer. Here we review the use of zebrafish as potential in vivo models for paediatric brain tumour modelling, as well as catalogue the currently available zebrafish models used to study paediatric brain cancer pathophysiology, and discuss key findings, the unique attributes that these models add, current challenges and therapeutic significance. Full article
(This article belongs to the Special Issue Molecular Genetics and Epigenetics of Tumors)
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