2. Academic Validation
  3. Amlexanox, a selective inhibitor of IKBKE, generates anti-tumoral effects by disrupting the Hippo pathway in human glioblastoma cell lines

Amlexanox, a selective inhibitor of IKBKE, generates anti-tumoral effects by disrupting the Hippo pathway in human glioblastoma cell lines

  • Cell Death Dis. 2017 Aug 31;8(8):e3022. doi: 10.1038/cddis.2017.396.
Yang Liu 1 2 3,  Jie Lu 4,  Zhimeng Zhang 1 2 3,  Lin Zhu 5,  Shicai Dong 1 2 3,  Gaochao Guo 1 2 3,  Ruohong Li 1 2 3,  Yang Nan 1 2 3,  Kai Yu 1 2 3,  Yue Zhong 1 2 3,  Qiang Huang 1 2 3
Affiliations

Affiliations

  • 1 Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China.
  • 2 Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, China.
  • 3 Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, China.
  • 4 Department of Neurosurgery, Shandong Provincial Qianfoshan Hospital, Shandong, China.
  • 5 Department of Pathology, The Second People's Hospital of Liaocheng, Linqing, China.
PMID: 29048430 DOI: 10.1038/cddis.2017.396
Abstract

Glioblastoma multiforme (GBM) is the most prevalent form of malignant brain tumor. Amlexanox, a novel compound, has been shown to have anti-cancer potential. In this study, the anti-tumoral effects and the underlying mechanisms of amlexanox were investigated. Amlexanox significantly suppressed proliferation and invasion and induced Apoptosis in glioblastoma cells. Furthermore, we found that amlexanox altered the protein expression of the Hippo pathway by downregulating IKBKE. Our data indicates that IKBKE directly targets LATS1/2 and induces degradation of LATS1/2, thereby inhibiting the activity of the Hippo pathway. In vivo results further confirmed the tumor inhibitory effect of amlexanox via the downregulation of IKBKE, and amlexanox induced no apparent toxicity. Collectively, our studies suggest that amlexanox is a promising therapeutic agent for the treatment of GBM.

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