Role of Borneol Induced Autophagy in Enhancing Radiosensitivity of Malignant Glioma.

Front Oncol

Department of Pharmacy, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, China.

Published: November 2021

AI Article Synopsis

  • - Gliomas are challenging brain cancers that are hard to treat, often requiring surgery and radiation, but these cells frequently resist radiation, leading to poor outcomes.
  • - The study explored how borneol can enhance the effectiveness of radiation therapy on glioma cells, finding that it significantly slows down cell growth and promotes autophagy (the process of clearing out damaged cells).
  • - Borneol was shown to disrupt key signaling pathways related to tumor growth, specifically the mTORC1/eIF4E/HIF-1α axis, thereby increasing the levels of proteins associated with autophagy (beclin-1 and LC3) and reducing glioma cell proliferation.

Article Abstract

Glioma is the common primary craniocerebral malignancy with unfavorable prognosis. It is currently treated by surgical resection supplemented by radiotherapy, although the resistance of glioma cells to radiation limits the therapeutic outcomes. The aim of the present study was to determine the potential radiosensitizing effects of borneol and the underlying mechanisms. We found that borneol administration along with radiotherapy significantly inhibited the growth of primary glioma cells and . Furthermore, borneol markedly increased the number of autophagosomes in the glioma cells, which coincided with increased expression of beclin-1 and LC3. And the combination of borneol and radiation exposure significantly decreased the expression levels of HIF-1α, mTORC1 and eIF4E. In addition, silencing mTORC1 and eIF4E upregulated Beclin-1 and LC3 and decreased the expression of HIF-1α, thereby inhibiting tumor cell proliferation. Our findings suggest that borneol sensitizes glioma cells to radiation by inducing autophagy inhibition of the mTORC1/eIF4E/HIF-1α regulatory axis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8668811PMC
http://dx.doi.org/10.3389/fonc.2021.749987DOI Listing

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