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Biomolecules
Special Issues
Novel Indications of Epigenetic Therapy in Cancer
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Novel Indications of Epigenetic Therapy in Cancer

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Genetics".

Deadline for manuscript submissions: closed (10 January 2022) | Viewed by 13371

Special Issue Editor

Dr. Olga Ostrovsky

E-Mail Website
Guest Editor
Department of Surgery, Cooper University Hospital, Camden, NJ, USA
Interests: regenerative medicine; stem cell therapy; tissue regeneration; cell growth control; cancer; epigenetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recently, cancer research has undergone a rapid development in novel strategies and efficacious treatments in the realm of oncology. Unfortunately, traditional cancer treatments—such as radiation, cytoreductive surgery, and classic chemotherapy—are not successful at eradicating disease for the majority of patients, especially those who present at advanced stages. In fact, high mortality and treatment failure rates are due to fast-developing chemoresistance. Furthermore, recent studies have exposed a critical role for the tumorigenic microenvironment aiding the support of tumor propagation, metastasis, and chemoresistance. Therefore, there is an imminent need for the development of novel therapeutic strategies that not only improve the efficacy of targeted tumor growth but also the ability to circumvent the grave chemoresistance problem.

Over the last decade, the study of epigenetics in variable types of tumors has gained tremendous attention. Epigenetic modifications such as DNA methylation and histone deacetylation have led to cancer progression, metastases, and an increase in chemoresistance in various oncologic subtypes. Unlike genetic mutations, which cannot be altered, epigenetically-induced alterations are promising targets. This has led to the advent of histone deacetylase inhibitors (HDACis) and DNA methyltransferase inhibitors (DNMTis). Genes encoding epigenetic regulators—both DNMTis and HDACis—are found in cancer and tend to drive tumorigenesis and resistance to standard chemotherapy treatments. Therefore, epigenetic therapy has great potential to not only suppress cancer propagation and metastasis but also to modify the cellular components of the same tumorigenic microenvironment that supports cancer growth, chemoresistance, and metastasis.

Moreover, the presence of aberrant epigenetic modification in tumors presents a unique opportunity for epigenetic therapy in the formulation of novel therapeutic strategies, in which tumor destruction is maximized with minimal damage to healthy tissue, therefore improving oncologic outcomes for cancer patients with less toxic side effects.

This Special Issue of Biomolecules aims to introduce and discuss novel applications of epigenetic therapy for the inhibition of cancer progression and modification of the tumorigenic microenvironment.

Dr. Olga Ostrovsky
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. Biomolecules is an international peer-reviewed open access monthly 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 2700 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

  • cancer therapy
  • epigenetics
  • chemoresistance
  • histone deacetylase inhibitors (HDACis)
  • DNA methyltransferase inhibitors (DNMTis)
  • tumor microenvironment

Published Papers (4 papers)

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Research

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10 pages, 677 KiB  
Article
Effects of Molecular Iodine/Chemotherapy in the Immune Component of Breast Cancer Tumoral Microenvironment
by Olga Cuenca-Micó, Evangelina Delgado-González, Brenda Anguiano, Felipe Vaca-Paniagua, Alejandra Medina-Rivera, Mauricio Rodríguez-Dorantes and Carmen Aceves
Biomolecules 2021, 11(10), 1501; https://doi.org/10.3390/biom11101501 - 12 Oct 2021
Cited by 4 | Viewed by 2858
Abstract
Molecular iodine (I2) induces apoptotic, antiangiogenic, and antiproliferative effects in breast cancer cells. Little is known about its effects on the tumor immune microenvironment. We studied the effect of oral (5 mg/day) I2 supplementation alone (I2) or together [...] Read more.
Molecular iodine (I2) induces apoptotic, antiangiogenic, and antiproliferative effects in breast cancer cells. Little is known about its effects on the tumor immune microenvironment. We studied the effect of oral (5 mg/day) I2 supplementation alone (I2) or together with conventional chemotherapy (Cht+I2) on the immune component of breast cancer tumors from a previously published pilot study conducted in Mexico. RNA-seq, I2 and Cht+I2 samples showed significant increases in the expression of Th1 and Th17 pathways. Tumor immune composition determined by deconvolution analysis revealed significant increases in M0 macrophages and B lymphocytes in both I2 groups. Real-time RT-PCR showed that I2 tumors overexpress T-BET (p = 0.019) and interferon-gamma (IFNγ; p = 0.020) and silence tumor growth factor-beta (TGFβ; p = 0.049), whereas in Cht+I2 tumors, GATA3 is silenced (p = 0.014). Preliminary methylation analysis shows that I2 activates IFNγ gene promoter (by increasing its unmethylated form) and silences TGFβ in Cht+I2. In conclusion, our data showed that I2 supplements induce the activation of the immune response and that when combined with Cht, the Th1 pathways are stimulated. The molecular mechanisms involved in these responses are being analyzed, but preliminary data suggest that methylation/demethylation mechanisms could also participate. Full article
(This article belongs to the Special Issue Novel Indications of Epigenetic Therapy in Cancer)
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14 pages, 2844 KiB  
Article
Computational Probing the Methylation Sites Related to EGFR Inhibitor-Responsive Genes
by Rui Yuan, Shilong Chen and Yongcui Wang
Biomolecules 2021, 11(7), 1042; https://doi.org/10.3390/biom11071042 - 16 Jul 2021
Cited by 2 | Viewed by 2243
Abstract
The emergence of drug resistance is one of the main obstacles to the treatment of lung cancer patients with EGFR inhibitors. Here, to further understand the mechanism of EGFR inhibitors in lung cancer and offer novel therapeutic targets for anti-EGFR-inhibitor resistance via the [...] Read more.
The emergence of drug resistance is one of the main obstacles to the treatment of lung cancer patients with EGFR inhibitors. Here, to further understand the mechanism of EGFR inhibitors in lung cancer and offer novel therapeutic targets for anti-EGFR-inhibitor resistance via the deep mining of pharmacogenomics data, we associated DNA methylation with drug sensitivities for uncovering the methylation sites related to EGFR inhibitor sensitivity genes. Specifically, we first introduced a grouped regularized regression model (Group Least Absolute Shrinkage and Selection Operator, group lasso) to detect the genes that were closely related to EGFR inhibitor effectiveness. Then, we applied the classical regression model (lasso) to identify the methylation sites associated with the above drug sensitivity genes. The new model was validated on the well-known cancer genomics resource: CTRP. GeneHancer and Encyclopedia of DNA Elements (ENCODE) database searches indicated that the predicted methylation sites related to EGFR inhibitor sensitivity genes were related to regulatory elements. Moreover, the correlation analysis on sensitivity genes and predicted methylation sites suggested that the methylation sites located in the promoter region were more correlated with the expression of EGFR inhibitor sensitivity genes than those located in the enhancer region and the TFBS. Meanwhile, we performed differential expression analysis of genes and predicted methylation sites and found that changes in the methylation level of some sites may affect the expression of the corresponding EGFR inhibitor-responsive genes. Therefore, we supposed that the effectiveness of EGFR inhibitors in lung cancer may be improved by methylation modification in their sensitivity genes. Full article
(This article belongs to the Special Issue Novel Indications of Epigenetic Therapy in Cancer)
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Review

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23 pages, 1526 KiB  
Review
Interplay between Epigenetics and Cellular Metabolism in Colorectal Cancer
by Xiaolin Zhang, Zhen Dong and Hongjuan Cui
Biomolecules 2021, 11(10), 1406; https://doi.org/10.3390/biom11101406 - 25 Sep 2021
Cited by 4 | Viewed by 2716
Abstract
Cellular metabolism alterations have been recognized as one of the most predominant hallmarks of colorectal cancers (CRCs). It is precisely regulated by many oncogenic signaling pathways in all kinds of regulatory levels, including transcriptional, post-transcriptional, translational and post-translational levels. Among these regulatory factors, [...] Read more.
Cellular metabolism alterations have been recognized as one of the most predominant hallmarks of colorectal cancers (CRCs). It is precisely regulated by many oncogenic signaling pathways in all kinds of regulatory levels, including transcriptional, post-transcriptional, translational and post-translational levels. Among these regulatory factors, epigenetics play an essential role in the modulation of cellular metabolism. On the one hand, epigenetics can regulate cellular metabolism via directly controlling the transcription of genes encoding metabolic enzymes of transporters. On the other hand, epigenetics can regulate major transcriptional factors and signaling pathways that control the transcription of genes encoding metabolic enzymes or transporters, or affecting the translation, activation, stabilization, or translocation of metabolic enzymes or transporters. Interestingly, epigenetics can also be controlled by cellular metabolism. Metabolites not only directly influence epigenetic processes, but also affect the activity of epigenetic enzymes. Actually, both cellular metabolism pathways and epigenetic processes are controlled by enzymes. They are highly intertwined and are essential for oncogenesis and tumor development of CRCs. Therefore, they are potential therapeutic targets for the treatment of CRCs. In recent years, both epigenetic and metabolism inhibitors are studied for clinical use to treat CRCs. In this review, we depict the interplay between epigenetics and cellular metabolism in CRCs and summarize the underlying molecular mechanisms and their potential applications for clinical therapy. Full article
(This article belongs to the Special Issue Novel Indications of Epigenetic Therapy in Cancer)
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12 pages, 493 KiB  
Review
Can Cannabidiol Affect the Efficacy of Chemotherapy and Epigenetic Treatments in Cancer?
by Courtney Griffiths, James Aikins, David Warshal and Olga Ostrovsky
Biomolecules 2021, 11(5), 766; https://doi.org/10.3390/biom11050766 - 20 May 2021
Cited by 13 | Viewed by 4544
Abstract
The success of cannabinoids with chronic neuropathic pain and anxiety has been demonstrated in a multitude of studies. With the high availability of a non-intoxicating compound, cannabidiol (CBD), an over-the-counter medication, has generated heightened interest in its use in the field of oncology. [...] Read more.
The success of cannabinoids with chronic neuropathic pain and anxiety has been demonstrated in a multitude of studies. With the high availability of a non-intoxicating compound, cannabidiol (CBD), an over-the-counter medication, has generated heightened interest in its use in the field of oncology. This review focuses on the widespread therapeutic potential of CBD with regard to enhanced wound healing, lowered toxicity profiles of chemotherapeutics, and augmented antitumorigenic effects. The current literature is sparse with regard to determining the clinically relevant concentrations of CBD given the biphasic nature of the compound’s response. Therefore, there is an imminent need for further dose-finding studies in order to determine the optimal dose of CBD for both intermittent and regular users. We address the potential influence of regular or occasional CBD usage on therapeutic outcomes in ovarian cancer patients. Additionally, as the development of chemoresistance in ovarian cancer results in treatment failure, the potential for CBD to augment the efficacy of conventional chemotherapeutic and epigenetic drugs is a topic of significant importance. Our review is focused on the widespread therapeutic potential of CBD and whether or not a synergistic role exists in combination with epigenetic and classic chemotherapy medications. Full article
(This article belongs to the Special Issue Novel Indications of Epigenetic Therapy in Cancer)
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