Whole transcriptome and proteome analyses identify potential targets and mechanisms underlying tumor treating fields against glioblastoma

  • Cell Death Dis. 2022 Aug 18;13(8):721. doi: 10.1038/s41419-022-05127-7.
Shengchao Xu   #  1  2 ,  Chengke Luo   #  1  2 ,  Dikang Chen  3 ,  Lu Tang  4 ,  Ling Chen  5 ,  Zhixiong Liu  6  7
Affiliations
  • 1. Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
  • 2. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
  • 3. Hunan An Tai Kang Cheng Biotechnology Co., Ltd, Changsha, China.
  • 4. Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
  • 5. Department of Neurosurgery, Chinese People's Liberation Army of China (PLA) General Hospital, Medical School of Chinese PLA, Institute of Neurosurgery of Chinese PLA, 100853, Beijing, China. [email protected].
  • 6. Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. [email protected].
  • 7. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. [email protected].
  • # Contributed equally.
PMID: 35982032 DOI: 10.1038/s41419-022-05127-7
Abstract

Glioblastoma (GBM) is one of the most malignant types of brain Cancer. Tumor treating fields (TTFields) is the up-to-date treatment for GBM. However, its molecular mechanism requires additional investigation. Herein, a novel TTFields system was developed (CL-301A) and its efficiency in suppressing GBM cell proliferation and inducing cell Apoptosis was demonstrated. Through the whole proteomic and transcriptomic analyses, a multitude of differentially expressed proteins (1243), mRNAs (4191), miRtNAs (47), lncRNAs (4286), and circRNAs (13,903) were identified. Bioinformatic analysis indicated that TTFields mainly affected nuclear proteins and interrupt cell mitosis-related events. Moreover, the inhibition of Autophagy could significantly enhance the anti-GBM activity of TTFields. And CDK2-AS1 might be a target of TTFields to mediate cell cycle arrest via regulating CDK2 mRNA stability. This study provided valuable resources for understanding the mechanism of TTFields, which might further assist the investigation of TTFields in GBM treatment.

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