Fig 1: Dysfunction of mitosis after KIF11 knockdown by siRNAs. Detection of postmitotic cells (white arrow), premitotic cells (sky blue arrow), and apoptotic cells (black arrow) by live-cell imaging.
Fig 2: Inhibition of oral cancer cell growth by KIF11 knockdown. (A and B) Expression of KIF11 protein in HSC4 and FaDu cells transfected with siRNAs for KIF11 and control siRNAs. (C and D) MTT assay of HSC4 and FaDu cells transfected with siRNAs for KIF11 and control siRNAs. All assays were performed in triplicate. (E and F) Inhibition of cell growth after transfecting siRNAs using the colony formation assay.
Fig 3: Ndc80/Nuf2 concentrates dynamic Prc1 at kinetochores for spindle bipolarization.a Dynamic exchange of Prc1 at kinetochores. In oocytes at prometaphase I (1.5 h after NEBD), SunTag-Prc1 (24xGCN4-Prc1 coexpressed with scFv-sfGFP, green) signals at kinetochores were bleached, and the recovery was monitored (n = 5, 5, 5 kinetochores). Note that the recovery curve of SunTag-Prc1 signals indicates the turnover of Prc1 at kinetochores rather than the turnover of scFv on 24xGCN4 in this time range, which was confirmed by Ndc80-SunTag (Ndc80-24xGCN4 coexpressed with scFv-sfGFP) exhibiting similar recovery curves to Ndc80-sfGFP. See also Supplementary Movie 7. b Kif11-dependent Prc1 enrichment along kinetochore-proximal microtubules of the bipolar spindle. Control or monastrol-treated oocytes at metaphase I (4–6 h after NEBD) were stained for Prc1 (green), microtubules (magenta), and DNA (Hoechst33342, blue). The oocytes were treated with a cold buffer for 1 min before fixation to facilitate antibody penetration into the spindle. Prc1 signals along kinetochore-proximal microtubule bundles were measured, and their ratio to microtubule signals was calculated (n = 25, 25 locations from 5, 5 oocytes. Three independent experiments were performed). ****p < 0.0001 (p = 8.1E-07) by two-tailed unpaired Student’s t-test. c Prc1 overexpression rescues spindle defects in Ndc80-deleted oocytes. Ndc80f/f Zp3-Cre oocytes overexpressing mEGFP-HURP, mEGFP-Kif11, mNeonGreen-HSET, or mNeonGreen-Prc1 were immunostained at metaphase I (5.5 h after NEBD). Spindle shapes were reconstructed in 3D and categorized (n = 29, 18, 18, 18, 24 oocytes from three independent experiments). ****p < 0.0001 (p = 5.1E-05) by two-tailed unpaired Student’s t-test. n.s., not significant. Scale bars, 10 µm. Mean +/- SD are presented in a–c.
Fig 4: Induction of apoptosis by KIF11 knockdown. (A and B) Population of cells at each phase using flow cytometric analysis of HSC4 and FaDu cells after transfecting siKIF11 or si-control. (C and D) Percentage of apoptotic HSC4 and FaDu cells after transfecting si-KIF11 or si-control. (E and F) Detection of apoptotic cells after transfecting si-KIF11 or si-control (apoptotic cells are stained with green fluorescence).
Fig 5: Association of KIF11 expression with poor prognosis in oral cancer tissues. (A) Immunohistochemical staining pattern of KIF11 protein in representative oral cancer tissues. Representative examples for strong, weak, and absent KIF11 expressions in oral cancer tissues and healthy tongue tissue (original magnification, ×100). (B) Kaplan-Meier analysis of survival in patients with oral cancer according to KIF11 expression.
Supplier Page from MilliporeSigma for Anti-KIF11 antibody produced in rabbit