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The Mechanisms of Both Epigenetic Drugs and Epigenetic Modifiers Induced Tumor Cell Death

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 July 2021) | Viewed by 14709

Special Issue Editor

Prof. Dr. Daniela Trisciuoglio

E-Mail Website
Guest Editor
Department of Research, Advanced Diagnostics and Technological Innovation, Regina Elena National Cancer Institute, Rome, Italy
Interests: cancer; epigenetic drugs; protein acetylation; cell death and autophagy; combination therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epigenetic modifications, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs, recognized for playing a fundamental role in cancer transformation and progression. These epigenetic aberrations regulate gene activity beyond the underlying sequence.

As a consequence, they also favor cell survival to drug by aberrant regulation of drug transporters, DNA-repair enzymes and pro-apoptotic factors expression, thus rendering cytotoxic and targeted drugs ineffective and allow selection of rare drug-resistant tumor cells. Moreover, the epigenetic modifiers have a direct effect on cell viability, affecting signaling pathway controlling cell survival or demise.

Given the importance of epigenetic marks and modifier in tumorigenesis, the study of the biological role and availability of corresponding inhibitors has attracted extensive attention in cancer field.

The aim of this Special Issue is to provide a broad overview on the topic of “Cancer Epigenetics and Epigenetic drugs” in the context of human cancer, drug resistance, and therapy. In particular, it is devoted to explore the link between epigenetic modifiers or epidrugs and cell death mechanism, and put forward an otherwise poorly understood role for epigenetic drugs as cell death inducers.

Prof. Dr. Daniela Trisciuoglio
Guest Editor

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Keywords

  • epigenetic inhibitors
  • combination therapy
  • apoptosis
  • autophagy
  • necroptosis
  • immunogenic cell death
  • cell death

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Published Papers (4 papers)

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Research

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18 pages, 4750 KiB  
Article
Protein Arginine Methyltransferase (PRMT) Inhibitors—AMI-1 and SAH Are Effective in Attenuating Rhabdomyosarcoma Growth and Proliferation in Cell Cultures
by Joanna Janisiak, Patrycja Kopytko, Marta Tkacz, Dorota Rogińska, Magdalena Perużyńska, Bogusław Machaliński, Andrzej Pawlik and Maciej Tarnowski
Int. J. Mol. Sci. 2021, 22(15), 8023; https://doi.org/10.3390/ijms22158023 - 27 Jul 2021
Cited by 13 | Viewed by 2598
Abstract
Rhabdomyosarcoma (RMS) is a malignant soft tissue cancer that develops mostly in children and young adults. With regard to histopathology, four rhabdomyosarcoma types are distinguishable: embryonal, alveolar, pleomorphic and spindle/sclerosing. Currently, increased amounts of evidence indicate that not only gene mutations, but also [...] Read more.
Rhabdomyosarcoma (RMS) is a malignant soft tissue cancer that develops mostly in children and young adults. With regard to histopathology, four rhabdomyosarcoma types are distinguishable: embryonal, alveolar, pleomorphic and spindle/sclerosing. Currently, increased amounts of evidence indicate that not only gene mutations, but also epigenetic modifications may be involved in the development of RMS. Epigenomic changes regulate the chromatin architecture and affect the interaction between DNA strands, histones and chromatin binding proteins, thus, are able to control gene expression. The main aim of the study was to assess the role of protein arginine methyltransferases (PRMT) in the cellular biology of rhabdomyosarcoma. In the study we used two pan-inhibitors of PRMT, called AMI-1 and SAH, and evaluated their effects on proliferation and apoptosis of RMS cells. We observed that AMI-1 and SAH reduce the invasive phenotype of rhabdomyosarcoma cells by decreasing their proliferation rate, cell viability and ability to form cell colonies. In addition, microarray analysis revealed that these inhibitors attenuate the activity of the PI3K-Akt signaling pathway and affect expression of genes related to it. Full article
(This article belongs to the Special Issue The Mechanisms of Both Epigenetic Drugs and Epigenetic Modifiers Induced Tumor Cell Death)
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14 pages, 2700 KiB  
Article
Genotoxicity and Epigenotoxicity of Carbazole-Derived Molecules on MCF-7 Breast Cancer Cells
by Claudio Luparello, Ilenia Cruciata, Andreas C. Joerger, Cory A. Ocasio, Rhiannon Jones, Raysa Khan Tareque, Mark C. Bagley, John Spencer, Martin Walker, Carol Austin, Tiziana Ferrara, Pietro D′Oca, Rossella Bellina, Rossella Branni and Fabio Caradonna
Int. J. Mol. Sci. 2021, 22(7), 3410; https://doi.org/10.3390/ijms22073410 - 26 Mar 2021
Cited by 8 | Viewed by 4175
Abstract
The carbazole compounds PK9320 (1-(9-ethyl-7-(furan-2-yl)-9H-carbazol-3-yl)-N-methylmethanamine) and PK9323 (1-(9-ethyl-7-(thiazol-4-yl)-9H-carbazol-3-yl)-N-methylmethanamine), second-generation analogues of PK083 (1-(9-ethyl-9H-carbazol-3-yl)-N-methylmethanamine), restore p53 signaling in Y220C p53-mutated cancer cells by binding to a mutation-induced surface crevice and acting as molecular chaperones. In the present paper, these three molecules have been tested [...] Read more.
The carbazole compounds PK9320 (1-(9-ethyl-7-(furan-2-yl)-9H-carbazol-3-yl)-N-methylmethanamine) and PK9323 (1-(9-ethyl-7-(thiazol-4-yl)-9H-carbazol-3-yl)-N-methylmethanamine), second-generation analogues of PK083 (1-(9-ethyl-9H-carbazol-3-yl)-N-methylmethanamine), restore p53 signaling in Y220C p53-mutated cancer cells by binding to a mutation-induced surface crevice and acting as molecular chaperones. In the present paper, these three molecules have been tested for mutant p53-independent genotoxic and epigenomic effects on wild-type p53 MCF-7 breast adenocarcinoma cells, employing a combination of Western blot for phospho-γH2AX histone, Comet assay and methylation-sensitive arbitrarily primed PCR to analyze their intrinsic DNA damage-inducing and DNA methylation-changing abilities. We demonstrate that small modifications in the substitution patterns of carbazoles can have profound effects on their intrinsic genotoxic and epigenetic properties, with PK9320 and PK9323 being eligible candidates as “anticancer compounds” and “anticancer epi-compounds” and PK083 a “damage-corrective” compound on human breast adenocarcinoma cells. Such different properties may be exploited for their use as anticancer agents and chemical probes. Full article
(This article belongs to the Special Issue The Mechanisms of Both Epigenetic Drugs and Epigenetic Modifiers Induced Tumor Cell Death)
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17 pages, 4272 KiB  
Article
Combination of ACY-241 and JQ1 Synergistically Suppresses Metastasis of HNSCC via Regulation of MMP-2 and MMP-9
by Ha Young Cho, Sang Wu Lee, Yu Hyun Jeon, Dong Hoon Lee, Go Woon Kim, Jung Yoo, So Yeon Kim and So Hee Kwon
Int. J. Mol. Sci. 2020, 21(18), 6873; https://doi.org/10.3390/ijms21186873 - 19 Sep 2020
Cited by 21 | Viewed by 3091
Abstract
Overexpression of histone deacetylase 6 (HDAC6) and bromodomain-containing protein 4 (BRD4) is related to aggressiveness of head and neck squamous carcinoma (HNSCC). Based on studies that HDAC6 and BRD4 are potential therapeutic targets of HNSCC, we hypothesized that the combination treatment of BET [...] Read more.
Overexpression of histone deacetylase 6 (HDAC6) and bromodomain-containing protein 4 (BRD4) is related to aggressiveness of head and neck squamous carcinoma (HNSCC). Based on studies that HDAC6 and BRD4 are potential therapeutic targets of HNSCC, we hypothesized that the combination treatment of BET inhibitor JQ1 and HDAC6-selective inhibitor ACY-241 could exhibit synergistic anticancer effects in human papillomavirus (HPV)-positive and HPV-negative HNSCC cells. In this study, HNSCC cell growth and viability were measured by CCK-8 assay, apoptosis was analyzed by flow cytometry, and metastasis was studied by wound healing and transwell assays. Furthermore, immunoblotting is conducted to investigate proteins that modulate apoptosis or metastasis. Here, we report that the combination of ACY-241 and JQ1 shows synergistic cell growth inhibition, viability reduction, and apoptosis induction in HNSCC cells through inactivation of AKT and NF-κB signaling. Importantly, we demonstrate that combined treatment of ACY-241 and JQ1 synergistically suppresses TNF-α-induced migration and invasion via dysregulating matrix metalloproteinase (MMP)-2, MMP-9, and MT1-MMP. Overall, the combination of ACY-241 and JQ1 significantly suppresses proliferation and metastasis in HPV-positive and HPV-negative HNSCC. Collectively, these findings suggest that the co-inhibition of BET and HDAC6 can be a new therapeutic strategy in HNSCC. Full article
(This article belongs to the Special Issue The Mechanisms of Both Epigenetic Drugs and Epigenetic Modifiers Induced Tumor Cell Death)
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Review

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11 pages, 687 KiB  
Review
Garcinol—A Natural Histone Acetyltransferase Inhibitor and New Anti-Cancer Epigenetic Drug
by Patrycja Kopytko, Katarzyna Piotrowska, Joanna Janisiak and Maciej Tarnowski
Int. J. Mol. Sci. 2021, 22(6), 2828; https://doi.org/10.3390/ijms22062828 - 11 Mar 2021
Cited by 45 | Viewed by 4215
Abstract
Garcinol extracted from Garcinia indica fruit peel and leaves is a polyisoprenylated benzophenone. In traditional medicine it was used for its antioxidant and anti-inflammatory properties. Several studies have shown anti-cancer properties of garcinol in cancer cell lines and experimental animal models. Garcinol action [...] Read more.
Garcinol extracted from Garcinia indica fruit peel and leaves is a polyisoprenylated benzophenone. In traditional medicine it was used for its antioxidant and anti-inflammatory properties. Several studies have shown anti-cancer properties of garcinol in cancer cell lines and experimental animal models. Garcinol action in cancer cells is based on its antioxidant and anti-inflammatory properties, but also on its potency to inhibit histone acetyltransferases (HATs). Recent studies indicate that garcinol may also deregulate expression of miRNAs involved in tumour development and progression. This paper focuses on the latest research concerning garcinol as a HAT inhibitor and miRNA deregulator in the development and progression of various cancers. Garcinol may be considered as a candidate for next generation epigenetic drugs, but further studies are needed to establish the precise toxicity, dosages, routes of administration, and safety for patients. Full article
(This article belongs to the Special Issue The Mechanisms of Both Epigenetic Drugs and Epigenetic Modifiers Induced Tumor Cell Death)
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