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Taniguchi, Keisuke; Konishi, Hiroaki; Yoshinaga, Akiko; Tsugane, Momomi; Takahashi, Hiroyuki; Nishisaka, Fukiko; Shishido, Yoshiyuki; Asai, Akira
Scientific reports, 03/2021, Letnik: 11, Številka: 1Journal Article
Signal transducer and activator of transcription 3 (STAT3) plays a critical role in regulating cell growth, survival, and metastasis. STAT3 signaling is constitutively activated in various types of hematologic or solid malignancies. YHO-1701 has been developed as an orally available STAT3 inhibitor. Herein, YHO-1701 in combination with molecular-targeted agents was evaluated. Additive or synergistic effects were observed in a broad spectrum of "combination treatment + cell line" pairs. Of particular interest was the synergistic effect observed when YHO-1701 was combined with imatinib or dasatinib breakpoint cluster region-abelson (BCR-ABL) inhibitors, osimertinib epidermal growth factor receptor (EGFR) inhibitor, crizotinib, alectinib, or ceritinib anaplastic lymphoma kinase (ALK) inhibitors. The results further showed a close relationship between these synergistic effects and the cellular levels of the key molecules involved in the target pathways for YHO-1701 and each combination drug. The combination of YHO-1701 with alectinib resulted in significantly greater antitumor activity without exhibiting body weight loss in an NCI-H2228 echinoderm microtubule-associated protein-like 4 (EML4)-ALK fusion xenograft mouse model. Our results strongly suggest that the logical strategy in combination with the novel STAT3 inhibitor YHO-1701 and other mechanistically different targeted agents, could be a promising approach in future clinical settings.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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