scholarly journals Histone Deacetylase Inhibitors Romidepsin and Vorinostat Promote Hepatitis B Virus Replication by Inducing Cell Cycle Arrest

2021 ◽  
Vol 000 (000) ◽  
pp. 000-000
Author(s):  
Yang Yang ◽  
Yu Yan ◽  
Zhen Chen ◽  
Jie Hu ◽  
Kai Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Cell Cycle Arrest ◽  
Histone Deacetylase ◽  
Virus Replication ◽  
Histone Deacetylase Inhibitors ◽  
Cycle Arrest ◽  
B Virus

scholarly journals Histone Deacetylase Inhibitors: A Promising Therapeutic Alternative for Endometrial Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Iason Psilopatis ◽  
Alexandros Pergaris ◽  
Constantinos Giaginis ◽  
Stamatios Theocharis
Keyword(s):  
Cell Cycle ◽  
Endometrial Cancer ◽  
Endometrial Carcinoma ◽  
Histone Acetylation ◽  
Cell Cycle Arrest ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
The United States ◽  
Carcinoma Cells ◽  
Cycle Arrest

Endometrial carcinoma is the most common malignant tumor of the female genital tract in the United States. Epigenetic alterations are implicated in endometrial cancer development and progression. Histone deacetylase inhibitors are a novel class of anticancer drugs that increase the level of histone acetylation in many cell types, thereby inducing cell cycle arrest, differentiation, and apoptotic cell death. This review is aimed at determining the role of histone acetylation and examining the therapeutic potential of histone deacetylase inhibitors in endometrial cancer. In order to identify relevant studies, a literature review was conducted using the MEDLINE and LIVIVO databases. The search terms histone deacetylase, histone deacetylase inhibitor, and endometrial cancer were employed, and we were able to identify fifty-two studies focused on endometrial carcinoma and published between 2001 and 2021. Deregulation of histone acetylation is involved in the tumorigenesis of both endometrial carcinoma histological types and accounts for high-grade, aggressive carcinomas with worse prognosis and decreased overall survival. Histone deacetylase inhibitors inhibit tumor growth, enhance the transcription of silenced physiologic genes, and induce cell cycle arrest and apoptosis in endometrial carcinoma cells both in vitro and in vivo. The combination of histone deacetylase inhibitors with traditional chemotherapeutic agents shows synergistic cytotoxic effects in endometrial carcinoma cells. Histone acetylation plays an important role in endometrial carcinoma development and progression. Histone deacetylase inhibitors show potent antitumor effects in various endometrial cancer cell lines as well as tumor xenograft models. Additional clinical trials are however needed to verify the clinical utility and safety of these promising therapeutic agents in the treatment of patients with endometrial cancer.

scholarly journals Modulation of translation factor's gene expression by histone deacetylase inhibitors in breast cancer cells

2005 ◽  
Vol 43 (2) ◽  
Author(s):  
João Gonçalves ◽  
Joana Malta-Vacas ◽  
Monette Louis ◽  
Laurent Brault ◽  
Denyse Bagrel ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Expression Patterns ◽  
Mrna Levels ◽  
Cycle Arrest ◽  
Translation Factors ◽  
Mcf 7

AbstractThe histone deacetylase inhibitors sodium butyrate (NaBu) and trichostatin A (TSA) exhibit anti-proliferative activity by causing cell cycle arrest and apoptosis. The mechanisms by which NaBu and TSA cause apoptosis and cell cycle arrest are not yet completely clarified, although these agents are known to modulate the expression of several genes including cell-cycle- and apoptosis-related genes. The enzymes involved in the process of translation have important roles in controlling cell growth and apoptosis, and several of these translation factors have been described as having a causal role in the development of cancer. The expression patterns of the translation mechanism, namely of the elongation factors eEF1A1 and eEF1A2, and of the termination factors eRF1 and eRF3, were studied in the breast cancer cell line MCF-7 by real-time quantitative reverse transcription-polymerase chain reaction after a 24-h treatment with NaBu and TSA. NaBu induced inhibition of translation factors' transcription, whereas TSA caused an increase in mRNA levels. Thus, these two agents may modulate the expression of translation factors through different pathways. We propose that the inhibition caused by NaBu may, in part, be responsible for the cell cycle arrest and apoptosis induced by this agent in MCF-7 cells.

scholarly journals Histone deacetylase inhibitors vorinostat and panobinostat induce G1 cell cycle arrest and apoptosis in multidrug resistant sarcoma cell lines

Oncotarget ◽  
2017 ◽  
Vol 8 (44) ◽  
pp. 77254-77267 ◽  
Author(s):  
Eva Bernhart ◽  
Nicole Stuendl ◽  
Heike Kaltenegger ◽  
Christian Windpassinger ◽  
Nicholas Donohue ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Histone Deacetylase ◽  
Cell Lines ◽  
Histone Deacetylase Inhibitors ◽  
Multidrug Resistant ◽  
Sarcoma Cell ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

T-cell lymphoma as a model for the use of histone deacetylase inhibitors in cancer therapy: impact of depsipeptide on molecular markers, therapeutic targets, and mechanisms of resistance

Blood ◽  
2004 ◽  
Vol 103 (12) ◽  
pp. 4636-4643 ◽  
Author(s):  
Richard L. Piekarz ◽  
Robert W. Robey ◽  
Zhirong Zhan ◽  
Ganesh Kayastha ◽  
Anousheh Sayah ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Cell ◽  
Cell Cycle Arrest ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Cell Lymphoma ◽  
Chemotherapeutic Agents ◽  
T Cell Lymphoma ◽  
Molecular Response ◽  
Cycle Arrest

Abstract Depsipeptide (FK228) is a novel histone deacetylase inhibitor currently in clinical trials and the first to demonstrate clinical activity in patients. Responses have been observed in patients with T-cell lymphomas, despite prior treatment with multiple chemotherapeutic agents. To better understand the effects of histone deacetylase inhibitors on T-cell lymphoma, the human T-cell lymphoma cell line HUT78 was tested for sensitivity and molecular response to depsipeptide. Treatment with depsipeptide, as well as other histone deacetylase inhibitors, caused induction of histone acetylation, induction of p21 expression, and substantial apoptosis without significant cell cycle arrest. Treatment with the caspase inhibitor z-VAD-fmk significantly inhibited depsipeptide-induced apoptosis, enabling detection of cell cycle arrest. Treatment with depsipeptide increased expression of the interleukin-2 (IL-2) receptor, and combination with the IL-2 toxin conjugate denileukin diftitox resulted in more than additive toxicity. Cells selected for resistance to depsipeptide overexpressed the multidrug resistance pump, P-glycoprotein (Pgp). However, cells selected for resistance to depsipeptide in the presence of a Pgp inhibitor had a Pgp-independent mechanism of resistance. These studies confirm the activity of depsipeptide in a T-cell lymphoma model and suggest a general sensitivity of T-cell lymphoma to histone deacetylase inhibitors, an emerging new class of anticancer agents. (Blood. 2004;103:4636-4643)

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