Journal
BIOMOLECULES
Volume 9, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/biom9100550
Keywords
brusatol; STAT3 inhibitor; apoptosis; HNSCC
Categories
Funding
- National Research Foundation of Korea (NRF) - Korean government (MSIP) [NRF-2017M3A9E4065333, 2018R1D1A1B07042969]
- University Grants Commission
- Institution of Excellence, University of Mysore
- National Research Foundation of Korea [2018R1D1A1B07042969] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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STAT3 is a latent transcription factor that plays a vital role in the transmission of extracellular signal from receptors to the nucleus. It has been regarded as a master transcription factor due to its role in the regulation of a broad spectrum of genes, which can contribute to oncogenesis. Persistent activation of STAT3 and deregulation of its signaling has been observed in various human cancers including head and neck squamous cell carcinoma (HNSCC). In the present work, we identified brusatol (BT) as a potential blocker of STAT3 signaling pathway in diverse HNSCC cells. The data from the cell-based experiments suggested that BT-induced cytotoxicity and abrogated the activation of STAT3 and that of upstream kinases such as JAK1, JAK2, and Src. It reduced the levels of nuclear STAT3 and its DNA binding ability. BT treatment increased annexin-V-positive cells, promoted procaspase-3 and PARP cleavage, and downregulated the mRNA and protein expression of diverse proteins (Bcl-2, Bcl-xl, survivin) in HNSCC cells. Taken together, brusatol can function as a promising inhibitor targeting STAT3 signaling pathway in HNSCC.
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