2. Academic Validation
  3. STAT3 phosphorylation inhibitor Bt354 exhibits anti-neoplastic activity in glioblastoma multiforme cells

STAT3 phosphorylation inhibitor Bt354 exhibits anti-neoplastic activity in glioblastoma multiforme cells

  • Environ Toxicol. 2024 Jun;39(6):3292-3303. doi: 10.1002/tox.24178.
Yi-Chun Chiang 1,  Padhmavathi Selvam 2,  You-Xuan Liu 2,  Po-Chang Shih 3,  Nan-Fu Chen 1 4,  Hsiao-Mei Kuo 5,  Hugo You-Hsien Lin 6 7,  Zhi-Hong Wen 2,  Wu-Fu Chen 2 5
Affiliations

Affiliations

  • 1 Department of Surgery, Division of Neurosurgery, Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan.
  • 2 Department of Marine Biotechnology and Resources, National Sun Yat-Sen University, Kaohsiung, Taiwan.
  • 3 Institute of BioPharmaceutical Sciences, National Sun Yat-sen University, Kaohsiung, Taiwan.
  • 4 Institute of Medical Science and Technology, National Sun Yat-sen University, Kaohsiung, Taiwan.
  • 5 Department of Neurosurgery, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University, College of Medicine, Kaohsiung, Taiwan.
  • 6 Department of Internal Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung, Taiwan.
  • 7 Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
PMID: 38415901 DOI: 10.1002/tox.24178
Abstract

The high mortality rate of glioblastoma multiforme (GBM), a lethal primary brain tumor, is attributable to postsurgical recurrence. STAT3, an oncogenic protein, is a signal transducer and transcription activator encourages Cancer cell migration and proliferation, which results in resistance to therapy. STAT3 inhibition reduces Cancer metastasis and improves patient prognosis. Bt354, a small molecule STAT Inhibitor, exhibits significant cytotoxic and anti-proliferative activities against certain Cancer types. Here, we demonstrated that exposure of GBM cells (U87 MG) to Bt354 had a significant, concentration-dependent growth suppression. Bt354 also induced Apoptosis and downregulated the expression of the epithelial-mesenchymal transition genes. Therefore, this study suggests the potential of Bt354 for treating GBM owing to its ability to induce cytotoxicity.

Keywords

Bt354; STAT3; epithelial‐mesenchymal transition; glioblastoma; invasion; signaling.

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