» Articles » PMID: 26426056

Epigenetic Therapy for Solid Tumors: Highlighting the Impact of Tumor Hypoxia

Overview
Journal Genes (Basel)
Publisher MDPI
Date 2015 Oct 2
PMID 26426056
Citations 24
Authors
Affiliations
Soon will be listed here.
Abstract

In the last few decades, epigenetics has emerged as an exciting new field in development and disease, with a more recent focus towards cancer. Epigenetics has classically referred to heritable patterns of gene expression, primarily mediated through DNA methylation patterns. More recently, it has come to include the reversible chemical modification of histones and DNA that dictate gene expression patterns. Both the epigenetic up-regulation of oncogenes and downregulation of tumor suppressors have been shown to drive tumor development. Current clinical trials for cancer therapy include pharmacological inhibition of DNA methylation and histone deacetylation, with the aim of reversing these cancer-promoting epigenetic changes. However, the DNA methyltransferase and histone deacetylase inhibitors have met with less than promising results in the treatment of solid tumors. Regions of hypoxia are a common occurrence in solid tumors. Tumor hypoxia is associated with increased aggressiveness and therapy resistance, and importantly, hypoxic tumor cells have a distinct epigenetic profile. In this review, we provide a summary of the recent clinical trials using epigenetic drugs in solid tumors, discuss the hypoxia-induced epigenetic changes and highlight the importance of testing the epigenetic drugs for efficacy against the most aggressive hypoxic fraction of the tumor in future preclinical testing.

Citing Articles

HIF1α-mediated transactivation of WTAP promotes AML cell proliferation via mA-dependent stabilization of KDM4B mRNA.

Shao Y, Li Y, Li M, Wang L, Zhou H, Liu D Leukemia. 2023; 37(6):1254-1267.

PMID: 37087529 DOI: 10.1038/s41375-023-01904-1.


Decitabine-induced DNA methylation-mediated transcriptomic reprogramming in human breast cancer cell lines; the impact of DCK overexpression.

Buocikova V, Tyciakova S, Pilalis E, Mastrokalou C, Urbanova M, Matuskova M Front Pharmacol. 2022; 13:991751.

PMID: 36278182 PMC: 9585938. DOI: 10.3389/fphar.2022.991751.


Blood Stasis Syndrome Accelerates the Growth and Metastasis of Breast Cancer by Promoting Hypoxia and Immunosuppressive Microenvironment in Mice.

Jin L, Tang B, Liu X, Mao W, Xia L, Du Y J Immunol Res. 2022; 2022:7222638.

PMID: 35711625 PMC: 9197668. DOI: 10.1155/2022/7222638.


Blockade LAT1 Mediates Methionine Metabolism to Overcome Oxaliplatin Resistance under Hypoxia in Renal Cell Carcinoma.

Xu Q, Liu Y, Sun W, Song T, Jiang X, Zeng K Cancers (Basel). 2022; 14(10).

PMID: 35626154 PMC: 9139506. DOI: 10.3390/cancers14102551.


JmjC-KDMs KDM3A and KDM6B modulate radioresistance under hypoxic conditions in esophageal squamous cell carcinoma.

Macedo-Silva C, Miranda-Goncalves V, Lameirinhas A, Lencart J, Pereira A, Lobo J Cell Death Dis. 2020; 11(12):1068.

PMID: 33318475 PMC: 7736883. DOI: 10.1038/s41419-020-03279-y.


References
1.
Sarkar S, Horn G, Moulton K, Oza A, Byler S, Kokolus S . Cancer development, progression, and therapy: an epigenetic overview. Int J Mol Sci. 2013; 14(10):21087-113. PMC: 3821660. DOI: 10.3390/ijms141021087. View

2.
Shu X, Li L, Ji M, Cheng Y, Ying J, Fan Y . FEZF2, a novel 3p14 tumor suppressor gene, represses oncogene EZH2 and MDM2 expression and is frequently methylated in nasopharyngeal carcinoma. Carcinogenesis. 2013; 34(9):1984-93. DOI: 10.1093/carcin/bgt165. View

3.
Shahrzad S, Bertrand K, Minhas K, Coomber B . Induction of DNA hypomethylation by tumor hypoxia. Epigenetics. 2007; 2(2):119-25. DOI: 10.4161/epi.2.2.4613. View

4.
Whitehead R, Rankin C, Hoff P, Gold P, Billingsley K, Chapman R . Phase II trial of romidepsin (NSC-630176) in previously treated colorectal cancer patients with advanced disease: a Southwest Oncology Group study (S0336). Invest New Drugs. 2008; 27(5):469-75. PMC: 3024913. DOI: 10.1007/s10637-008-9190-8. View

5.
Olcina M, Foskolou I, Anbalagan S, Senra J, Pires I, Jiang Y . Replication stress and chromatin context link ATM activation to a role in DNA replication. Mol Cell. 2013; 52(5):758-66. PMC: 3898930. DOI: 10.1016/j.molcel.2013.10.019. View