Picrasidine G decreases viability of MDA-MB 468 EGFR-overexpressing triple-negative breast cancer cells through inhibition of EGFR/STAT3 signaling pathway

• Published in: Bioorganic & Medicinal Chemistry Letters Vol. 27; no. 11; pp. 2608 - 2612
• Main Authors: Yamashita, Naoya, Kondo, Manami, Zhao, Shuai, Li, Wei, Koike, Kazuo, Nemoto, Kiyomitsu, Kanno, Yuichiro
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.06.2017; Elsevier BV
• Subjects: Alkaloids; Alkaloids - chemistry; Alkaloids - toxicity; Apoptosis; Apoptosis - drug effects; Breast cancer; Carbolines; Carbolines - chemistry; Carbolines - toxicity; Caspase; Caspase 3; Caspase 3 - metabolism; Cell Line, Tumor; Cell Survival; Cell Survival - drug effects; Epidermal growth factor receptor; ErbB Receptors; Female; G1 Phase Cell Cycle Checkpoints; G1 Phase Cell Cycle Checkpoints - drug effects; Humans; Interleukin-6; Interleukin-6 - pharmacology; Phosphorylation; Phosphorylation - drug effects; Poly(ADP-ribose) Polymerases; Poly(ADP-ribose) Polymerases - metabolism; Receptor, Epidermal Growth Factor - metabolism; Signal transducer and activator of transcription 3; Signal Transduction; Signal Transduction - drug effects; STAT3 Transcription Factor; STAT3 Transcription Factor - metabolism; Triple Negative Breast Neoplasms; Triple Negative Breast Neoplasms - metabolism; Triple Negative Breast Neoplasms - pathology; Caspase; Breast cancer; Epidermal growth factor receptor; Signal transducer and activator of transcription 3; Apoptosis

[Display omitted] •Picrasidine G decreased viability of EGFR-overexpressing triple-negative breast cancer cells.•Picrasidine G increased caspase-dependent apoptotic cells.•Picrasidine G inhibited EGF-induced STAT3 phosphorylation. Targeted therapy is unavailable for treating patients with triple-neg...