Fig. 1: Highly expressed ANLN participates in ESCC malignant progression by promoting cytokinesis and proliferation. | Cell Death & Differentiation

Fig. 1: Highly expressed ANLN participates in ESCC malignant progression by promoting cytokinesis and proliferation.

From: Targeting USP10 induces degradation of oncogenic ANLN in esophageal squamous cell carcinoma

Fig. 1

A Representative image of ANLN immunohistochemical staining in ESCC and normal tissues (scale 200 and 50 μm). B ANLN expression in 104 ESCC tissues and normal tissues. C Kaplan–Meier curve analysis of the correlation between ANLN protein expression and overall survival of 104 ESCC patients. D Western blot analysis of ANLN knockdown by different siRNAs in KYSE150 and KYSE510 cells. E, F Effect of ANLN on ESCC cell proliferation was determined by colony formation (E) and an xCELLigence Real-Time Cell Analyzer (RTCA) system (F). G Cells after ANLN knockdown for 60 h were analyzed by flow cytometry. H KYSE150 cells were transfected with control or ANLN siRNA for 48 h. ANLN and cell-cycle proteins were detected using western blotting. I KYSE150 cells stably expressing HA-vector or HA-ANLN was transfected with an ANLN 3′UTR siRNA pool, then treated with thymidine for 24 h, and released for 12 h to obtain cytokinesis cells. Cells were fixed and detected by immunofluorescence. J Mean intensity ratio of individual cells were plotted (F-Actin fluorescence at the equatorial cortex: pole). P < 0.0001 by Student’s t-test. Left: diagram showing locations of regions of calculation. K–L KYSE150 cells stably expressing HA-vector or HA-ANLN were transfected with an ANLN 3’UTR siRNA pool, then cyclin B1 and E2 expression was detected by western blotting, and cell proliferation was detected by colony formation. All data are representative of at least three independent experiments and the results were statistically analyzed using a t-test.

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