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Simultaneous Measurement of HDAC1 and HDAC6 Activity in HeLa Cells Using UHPLC-MS
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Simultaneous Measurement of HDAC1 and HDAC6 Activity in HeLa Cells Using UHPLC-MS

Published on: August 10, 2017

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Growth Suppression of Glioma Cells Using HDAC6 Inhibitor, Tubacin

Changjiang Yin1, Pibao Li2

  • 1Department of Neurosurgery, Shandong Province Third Hospital, Jinan, Shandong, China.

Open Medicine (Warsaw, Poland)
|May 31, 2018
PubMed

Insights

Inhibiting histone deacetylase 6 (HDAC6) with tubacin suppressed glioma cell growth and drug resistance by blocking autophagy. This approach, combined with temozolomide, enhanced glioma cell death, offering a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Autophagy is crucial for cancer cell metabolism and survival, particularly in glioma.
  • Autophagy acts as a protective mechanism for glioma cells against treatments like chemotherapy and radiation.
  • Targeting autophagy presents a potential strategy for glioma treatment.

Purpose of the Study:

  • To investigate the effect of inhibiting histone deacetylase 6 (HDAC6) on glioma cells.
  • To evaluate the role of tubacin, an HDAC6 inhibitor, in modulating autophagy and glioma cell viability.
  • To assess the combined effect of tubacin and temozolomide on glioma cell death.

Main Methods:

  • Utilized tubacin, a specific inhibitor of HDAC6.
  • Assessed the impact of tubacin on U251 and LN229 glioma cell lines.
  • Measured HDAC6 activity, autophagosome accumulation, and cell death.
  • Evaluated the combined efficacy of tubacin and temozolomide.

Main Results:

  • Tubacin inhibited the growth of U251 and LN229 glioma cells.
  • Tubacin treatment led to decreased HDAC6 activity and increased autophagosome accumulation.
  • HDAC6 inhibition resulted in autophagosome accumulation and glioma cell death.
  • Combined treatment with tubacin and temozolomide significantly increased glioma cell death.

Conclusions:

  • Inhibition of HDAC6 suppresses glioma cell growth and enhances drug sensitivity in vitro.
  • Autophagic suppression and impaired autophagosome-lysosome fusion are key mechanisms.
  • Targeting HDAC6-mediated autophagy offers a promising therapeutic avenue for glioma treatment.
Keywords:
AutophageDrug resistantGliomaHDAC6

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