HDAC10 and its implications in Sézary syndrome pathogenesis.

in Frontiers in cell and developmental biology by Monika Pieniawska, Karolina Rassek, Bogumiła Skwara, Magdalena Żurawek, Iwona Ziółkowska-Suchanek, Lydia Visser, Monique Lodewijk, Małgorzata Sokołowska-Wojdyło, Berenika Olszewska, Roman J Nowicki, Tomasz Stein, Aleksandra Dańczak-Pazdrowska, Adriana Polańska, Marta Szymoniak-Lipska, Natalia Rozwadowska, Katarzyna Iżykowska

TLDR

  • HDAC10 is overexpressed in Sézary syndrome and plays a role in cellular growth and survival, making it a potential therapeutic target.
  • Inhibition of HDAC10 increased the sensitivity of Sézary cells to chemotherapy, suggesting a promising approach for treatment.

Abstract

Cutaneous T-cell lymphomas (CTCL) are a group of rare hematological malignancies characterized by infiltration of malignant T-cells into the skin. Two main types of CTCL constitute of Mycosis Fungoides (MF), a more indolent form of the disease, and Sézary syndrome (SS), the aggressive and leukemic variant with blood involvement. Sézary syndrome presents a significant clinical challenge due to its very aggressive nature, poor prognosis, and treatment resistance, and to date, the disease remains incurable. Histone deacetylase inhibitors have gained attention in CTCL treatment with promising results, but they expose limited specificity and strong side effects. Recent genomic studies underscore the role of epigenetic modifiers in CTCL pathogenesis, prompting an investigation into HDAC10, a member of class IIb HDACs, in SS. HDAC10 was investigated in different cancers, revealing its involvement in cell cycle regulation, apoptosis, and autophagy, but its role in CTCL is unknown. In this study we aimed to determine the role of HDAC10 in SS, focusing on its cellular localization, role in cell growth, and therapeutic potential. We indicated that HDAC10 is overexpressed in SS patients and located mainly in the cytoplasm. Its overexpression leads to an inhibitory effect on apoptosis progression when exposed to the pro-apoptotic compound Camptothecin (CPT). Knockdown of HDAC10 resulted in reduced cell growth and induction of apoptosis and autophagy, highlighting its potential importance in CTCL pathogenesis. Whole transcriptome analysis indicated that HDAC10 is associated with crucial cancer-related pathways, for example, hematopoietic cell lineage, PI3K-Akt signaling pathway, Ras signaling pathway, MAPK signaling pathway or JAK-STAT signaling pathway, which are critical for the survival and proliferation of malignant T cells. Inhibition of HDAC10 with selective HDAC10i increased the sensitivity of Sézary cells to the pro-apoptotic CPT. Our findings demonstrate that HDAC10 plays a key role in the molecular background of Sézary syndrome, highlighting its importance in the cellular mechanisms of the disease.

Overview

  • The study aims to determine the role of HDAC10 in Sézary syndrome, focusing on its cellular localization, role in cell growth, and therapeutic potential.
  • The study used knockdown and inhibition methods to investigate the effects of HDAC10 on cell growth, apoptosis, and autophagy in Sézary syndrome patients.
  • The primary objective of the study is to understand the molecular background of Sézary syndrome and identify potential therapeutic targets for the disease.

Comparative Analysis & Findings

  • HDAC10 is overexpressed in Sézary syndrome patients and located mainly in the cytoplasm, suggesting a potential role in cell growth and survival.
  • Knockdown of HDAC10 reduced cell growth and induced apoptosis and autophagy, indicating its importance in CTCL pathogenesis.
  • HDAC10 inhibition increased the sensitivity of Sézary cells to the pro-apoptotic compound Camptothecin, suggesting a potential therapeutic approach for the disease.

Implications and Future Directions

  • The study's findings suggest that HDAC10 is a potential therapeutic target for Sézary syndrome, and its inhibition could increase the sensitivity of Sézary cells to chemotherapy.
  • Future studies should investigate the mechanisms by which HDAC10 regulates cellular processes in Sézary syndrome and explore potential combination therapy approaches.
  • Understanding the specific role of HDAC10 in CTCL pathogenesis could lead to the development of novel and effective treatments for the disease.