3-Formylchromone attenuates urethane-induced lung carcinogenesis and enhances gefitinib anti-tumor response via modulation of IL-6/JAK1/STAT3/cyclin D1 signaling

model revealed a significant down-regulation of IL-6 content in the lung, repressed phosphorylation and activation of JAK1/STAT3 signaling, and declined protein expression of the proliferation marker cyclin D1 by 3-formylchromone treatment, relative to urethane group. 3-Formylchromone/gefitinib combination therapy further improved the therapeutic management of lung cancer with markedly reduced number/size of tumor nodules and the pathological changes in the lung, along with the powerful interference with IL-6/JAK1/STAT3 signaling, relative to gefitinib-treated group. Collectively, 3-formylchromone exhibits anti-tumor effect and could enhance gefitinib efficacy against lung cancer, at least partly, through inhibition of IL-6/JAK1/STAT3/cyclin D1 signaling. Thus, it can be suggested as a promising modality to investigate the potential to improve the management of lung cancer and to overcome the reduced sensitivity to gefitinib on prolonged therapy.