Targeting colon cancer with the novel STAT3 inhibitor bruceantinol View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-10-22

AUTHORS

Ning Wei, Jun Li, Cheng Fang, Jin Chang, Vasiliki Xirou, Nick K. Syrigos, Benjamin J. Marks, Edward Chu, John C. Schmitz

ABSTRACT

STAT3, a transcriptional mediator of oncogenic signaling, is constitutively active in ~70% of human cancers. The development of STAT3 inhibitors remains an active area of research as no inhibitors have yet to be approved for the treatment of human cancer. Herein, we revealed that bruceantinol (BOL) is a novel STAT3 inhibitor demonstrating potent antitumor activity in in vitro and in vivo human colorectal cancer (CRC) models. BOL strongly inhibited STAT3 DNA-binding ability (IC50 = 2.4 pM), blocked the constitutive and IL-6-induced STAT3 activation in a dose- and time-dependent manner, and suppressed transcription of STAT3 target genes encoding anti-apoptosis factors (MCL-1, PTTG1, and survivin) and cell-cycle regulators (c-Myc). Structure–activity relationship studies demonstrated that the C15 side chain on BOL affected its ability to bind STAT3. Administration of 4 mg/kg BOL significantly inhibited CRC tumor xenografts [p < 0.001], but no effect was observed in a STAT3−/− tumor model. Additional studies showed that BOL effectively sensitized MEK inhibitors through repression of p-STAT3 and MCL-1 induction, known resistance mechanisms of MEK inhibition. Taken together, our findings suggest BOL is a novel therapeutic STAT3 inhibitor that can be used either alone or in combination with MEK inhibitors for the treatment of human CRC. More... »

PAGES

1676-1687

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41388-018-0547-y

DOI

http://dx.doi.org/10.1038/s41388-018-0547-y

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1107761860

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30348989


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