Fig 2: Effect of KIF11 or KIF15 depletion on growth of U-R or H-R cells.(A) Experimental procedure. (B) Evaluation of knockdown efficiency by immunoblotting. (C) KIF11 knockdown heavily compromised the growth of the U-R cells, while the growth of H-R cells was affected only when both KIF11 and KIF15 were depleted, suggesting their mutually compensatory relationship. Cell viability was shown relative to that for the cells treated with control siRNA.

Fig 3: Co-occurrence of hub gene alterations in NSCLC and ChIP-seq of histone and transcription factors in A549 cells. (A) Five pairs of hub genes tending to have concurrent CNAs in NSCLC. (B) The characteristic peaks (fold change over control) of H3K4me3 and H3K27ac at the promoter region of BUB1B, CDC6, CDC20, CDK1, NCAPG and KIF11. (C) The characteristic peaks (fold change over control) of MYC at the promoter region of BUB1B, CDK1 and CCNA2.

Fig 4: Survival analysis and ROC curve analysis of hub genes in NSCLC. (A) Kaplan-Meier survival curves of OS based on the hub genes (CDC6, KIAA0101, CDC20, BUB1B, CCNA2, NCAPG, KIF11, BUB1, CDK1) expression using the online bioinformatics tool Kaplan-Meier Plotter. (B–F) Individual ROC curve of hub genes according to the chip data of GSE19804, GSE43458 and GSE18842. (G) Combined ROC curve of hub genes according to the chip data of GSE19804, GSE43458 and GSE18842.

Fig 5: STLC-resistant bipolar spindle formation in U-R and H-R cells.(A) Cells were treated with 8 µM STLC for 5 h and spindle morphology was examined using immunofluorescence microscopy for a-tubulin. More than 100 metaphase spindles were counted for each condition and chi-square-test was performed to evaluate statistical significance of the difference in monopolar index. (B) Localization of KIF11 was examined using immunofluorescence microscopy. Some kinesin-5 was localized to the metaphase spindle in STLC-treated U-R cells, but was nearly absent in the spindle of STLC-treated H-R cells. Scale bar is 10 µm. Gray scale and green, kinesin-5; red, tubulin; blue, DNA.