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Fig. 4 | Clinical Epigenetics

Fig. 4

From: Histone demethylase JARID1B/KDM5B promotes aggressiveness of non-small cell lung cancer and serves as a good prognostic predictor

Fig. 4

JARID1B expression activates the c-Met signaling pathway, facilitates CSCs-like phenotype in NSCLC, and JARID1B knockdown increases sensitivity to chemotherapy. a The expression of JARID1B, c-Met, c-Myc, SOX2, KLF4, MAPK, STAT3, FAK, survivin in H441, and H441 tumorspheres (spheroids) were shown. β-Actin served as the loading control. b Tumorsphere formation assay showed the inhibitory effect of JARID1B knockdown on tumorsphere formation (upper panel) as well as on the expression of c-Met and c-Myc (lower panel). c Immunofluorescence staining showing that H441 tumorspheres had greater expression of JARID1B and SOX2, compared with their H441-parental counterparts. d Fluorescence-activated cell sorter (FACS) analysis demonstrated the reduction of Hoechst 33342 efflux in shJARID1B cells as compared to the control H441 cells. The percentages indicated the proportion of side-population (SP) cells. The gated R5 region (blue) represented the Hoechst stain effluxing SP cells. The SP cell proportion reduced with verapamil treatment. e Dual-color immunofluorescence showed the co-expression and co-localization of JARID1B (red) and Sox2 (green). DAPI (blue) is the nuclear marker. Their expression was significantly diminished in the JARID1B-knockdown H441 cells. f Western blot for JARID1B in the control H441 cells and in the shJARID1B H441 cells. The control and JARID1B-knockdown cells were treated with increasing concentration of g cisplatin or h doxorubicin for 24 h. Cell viability was measured by SRB assay. *p < 0.05

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