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Received: 15 March 2021 Revised: 15 November 2021 Accepted: 18 November 2021 DOI: 10.1111/jcmm.||ORIGINAL ARTICLEC1632 suppresses the migration and proliferation of non-smallcell lung cancer cells involving LIN28 and FGFR1 pathwayJing-yi Chen1| Yu-jing Chen1| Lu Liu1| Xiang-xiang Jin1| Zhe Shen1| Wen-bin Chen1| Teng Yang1| Si-bei Xu1| Guang-bao Wang1| Yi-nuo Cheng1| De-zhi Cheng2| Zhi-guo Liu1| Xiao-hui ZhengChemical Biology Analysis Center, College of Pharmaceutical Sciences, Wenzhou Health-related University, Wenzhou, Zhejiang, ChinaAbstractChemoresistance and migration represent significant obstacles within the therapy of nonsmall-cell lung cancer (NSCLC), which accounts for about 85 of lung cancer individuals in clinic. In the present study, we report that the compound C1632 is preferentially distributed inside the lung following oral administration in vivo with high bioavailability and restricted inhibitory effects on CYP450 isoenzymes. We discovered that C1632 could simultaneously inhibit the expression of LIN28 and block FGFR1 signalling transduction in NSCLC A549 and A549R cells, resulting in important decreases within the phosphorylation of focal adhesion kinase as well as the expression of matrix metalloproteinase-9. Consequently, C1632 effectively inhibited the migration and invasion of A549 and A549R cells. Meanwhile, C1632 substantially suppressed the cell viability along with the colony formation of A549 and A549R cells by inhibitin