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Pharmacological blockade of HDAC6 attenuates cancer progression by inhibiting IL-1β and modulating immunosuppressive

Ashutosh Mahale1, Ganesh Routholla2, S Lavanya1

  • 1Metabolic Disorders and Neuroscience Research laboratory, Department of Pharmacy, Birla Institute of Technology and Science-Pilani, Hyderabad Campus, India.

International Immunopharmacology
|March 28, 2024
PubMed
Summary

Histone deacetylase-6 (HDAC6) inhibitors, like Tubastatin A, show promise in treating oral squamous cell carcinoma (OSCC). These inhibitors regulate interleukin-1 beta (IL-1β) and the tumor microenvironment (TME), reducing OSCC progression and improving patient survival.

Keywords:
HDAC6IL-1βOSCCTubastatin A

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Interleukin-1 beta (IL-1β) is a key biomarker in oral squamous cell carcinoma (OSCC), with elevated levels in the tumor microenvironment (TME) correlating with poor patient survival.
  • Targeting IL-1β offers a potential therapeutic strategy for OSCC treatment.

Purpose of the Study:

  • To investigate the role of histone deacetylase-6 (HDAC6) inhibition in regulating IL-1β and the TME in OSCC.
  • To evaluate the therapeutic potential of HDAC6 inhibitors in OSCC progression.

Main Methods:

  • Utilized a 4-nitroquinoline (4-NQO) induced OSCC mouse model and 4-NQO & lipopolysaccharide (LPS) stimulated OSCC and fibroblast cell lines.
  • Administered Tubastatin A (TSA), an HDAC6 inhibitor, and assessed its effects on tumor histology, protein expression (HDAC6, IL-1β, caspase-1, acetylated-tubulin), and immune cell populations (MDSCs, M2/M1 macrophages).
  • Performed TCGA analysis on human OSCC data and in vitro experiments involving nocodazole to elucidate the mechanism of IL-1β regulation.

Main Results:

  • TSA treatment attenuated OSCC progression in mice, improving histology and reducing tumor burden.
  • TSA modulated the TME by downregulating myeloid-derived suppressor cells and M2 macrophages while increasing M1 macrophages.
  • TSA inhibited IL-1β release through tubulin acetylation, independent of IL-1β processing, suggesting a novel mechanism of action.

Conclusions:

  • HDAC6 inhibitors, such as TSA, demonstrate significant therapeutic potential in OSCC by modulating the TME and regulating IL-1β.
  • The findings highlight HDAC6 inhibition as a promising strategy for OSCC treatment, offering a novel approach to targeting cancer progression.