4.2 Article

HSP27 protects against ferroptosis of glioblastoma cells

Journal

HUMAN CELL
Volume 35, Issue 1, Pages 238-249

Publisher

SPRINGER JAPAN KK
DOI: 10.1007/s13577-021-00645-6

Keywords

Glioblastoma; HSP27; Ferroptosis; Phosphorylation; Erastin

Categories

Funding

  1. National Natural Science Foundation of China [82072764, 82001385]
  2. Fundamental Research Funds for the Central Universities [2042021kf0089]

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This study unveils novel molecular mechanisms of ferroptosis in glioma and identifies HSP27 as a negative regulator of ferroptosis and a potential target for the treatment of glioma.
Ferroptosis, as an new form of non-apoptotic regulated cell death, plays an important role in human cancers. Although it is reported that HSP27 is an novel regulator of ferroptosis in cancer, it remains unknown how HSP27 affects ferroptosis in glioma. In this study, we examined the effect of HSP27 on the ferroptosis of glioblasotma. HSP27 overexpression protects glioblastoma cells from erastin-induced ferroptosis while HSP27 depletion promotes erastin-induced ferroptosis of glioblastoma. Notably, HSP27 phosphorylation is required for the protective function of HSP27 in erastin-induced ferroptosis. Overall, our study reveal novel molecular mechanisms of ferroptosis in glioma and also identify HSP27 as a negative regulator of ferroptosis and a potential target for the treatment of glioma.

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