Fig 2: Intracellular paclitaxel concentrations were measured by (a, c) confocal microscopy and (b, d) flow cytometry after treating the Caski/Taxol cells with 80 μM Flutax-2 for 48 h following the knockdown of FOXM1 using (a, b) shRNAs or (c, d) inhibition of FOXM1 using Siomycin A. The results showed that intracellular paclitaxel concentrations were significantly increased following FOXM1 knockdown by shRNA or inhibition by Siomycin A, indicating the potential of Siomycin A to sensitize chemo-resistant cancer cells to paclitaxel. ∗∗∗P < 0.001. Caski/Taxol: paclitaxel-resistant Caski cells; shRNA: small interfering RNA; FOXM1: forkhead box M1.

Fig 3: Effect of chondroitin polymerizing factor (CHPF) on global gene expression. A, Heatmap representation of 635 differentially expressed genes (DEGs) in A549 cells infected with shCHPF or shCtrl. P<0.05 and fold-change >2 (red: upregulated genes; green: downregulated genes). B, Functional pathway enrichment of the DEGs was analyzed via Ingenuity Pathway Analysis. The x-axis represents the pathway. Statistical significance is shown on the y-axis and represents the inverse log of the P-value. C, The network was built on the basis of microarray data of lung cancer cells. Red represents upregulation and green represents downregulation. D, Western blotting analysis was applied to evaluate the expression of CDH1, FOXM1, RRM2, HIF1A, CCND1, MKI67, and TNFRSF10B in shCHPF and shCtrl lung cancer cells. Data are reported as means±SD. **P<0.01 (Student's t-test).

Fig 4: Propofol alleviated lung cancer cell progression by regulating FOXM1. (a) FOXM1 protein level was detected by Western blot in H1299 and A549 cells treated with various doses of propofol (5, 10, and 15 μg/ml) for 48 h. (b) The overexpression efficiency of FOXM1 was validated via Western blot. (c–j) H1299 and A549 cells transfected with pcDNA or FOXM1 were stimulated with propofol (10 μg/ml) for 48 h. (c) FOXM1 protein level; (d) cell viability; (e) number of colonies; (f) apoptosis rate; and (g) cell invasion were evaluated by corresponding methods. (h–j) Relative glucose consumption, lactate production and ATP/ADP ratios were measured using the appropriate kit. ***p < 0.001, ****p < 0.0001

Fig 5: Linc-ROR and FOXM1 are highly expressed in HNSCC cells and promote cell proliferation and invasion. (A) The expression of Linc-ROR and FOXM1 in HNOEC/HL-047 and TSCCA cells detected by RT-qPCR; (B) The protein expression of FOXM1 in HNOEC/HL-047 and TSCCA cells detected by Western blot; (C) The knockdown effects of Linc-ROR and FOXM1 detected by RT-qPCR; (D) The knockdown effects of FOXM1 detected by Western blot; (E) Proliferation ability of TSCCA cells after silencing Linc-ROR detected by monoclonal formation assay; (F) Proliferation ability of TSCCA cells after silencing FOXM1 by monoclonal formation assay; (G) Proliferation ability of TSCCA cells after silencing Linc-ROR detected by MTT assay; (H) Proliferation ability of TSCCA cells after silencing FOXM1 detected by MTT assay; (I) Invasion capacity of TSCCA cells after silencing Linc-ROR detected by Transwell assay; (J) Invasion capacity of TSCCA cells after silencing FOXM1 detected by Transwell assay. In panel (A, B), *p < 0.05, compared with the HNOEC/HL-047 cells, in panel (C–J), TSCCA cells transfected with sh-NC. All experiments were repeated three times.