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. 2021 Jan 12;11:644. doi: 10.1038/s41598-020-80060-3

Figure 1.

Figure 1

EPHA10 is required for tumorigenesis and metastasis of OSCC cells. (A) Expression of EPHA10 in 20 types of cancer versus corresponding normal tissues using the Oncomine database with the threshold of fold change ≥ 2, p ≤ 10–4, and gene rank ≥ top 10%. Red and blue, respectively, indicate the numbers of datasets with statistically significant increases and decreases in EPHA10 gene expression. (B) EPHA10 expression in human oral keratinocytes (HOK), immortalized dysplastic oral keratinocytes (DOK), and 7 OSCC cell lines was examined by western blotting. Protein levels were normalized to an internal control (α-tubulin). Relative ratios were determined by dividing the EPHA10 protein level in each cell type by that in HOK cells. (C) EPHA10 protein levels in LN1-1 cells expressing EPHA10-specific shRNA and vector control (pLKO-GFP) were determined by western blot. Protein levels were normalized to α-tubulin. Relative ratios were determined by dividing the EPHA10 protein level in each expression variant by that in the pLKO-GFP vector-expressing cells. (D) EPHA10 protein levels in LN1-1 cells expressing pLKO-GFP (green line), sh3 (dark green line), and sh5 (pink line) were determined by fluorescence activated cell sorting (FACS). Relative EPHA10 expression was determined by dividing the fluorescent intensity in each expression variant by that in the pLKO-GFP vector-expressing cells. (E) Tumor weights and volumes in mice orthotopically injected with LN1-1 pLKO-GFP (n = 9) or EPHA10 sh3 cells (n = 8). (F) Ki-67 expression by immunohistochemistry (IHC) in LN1-1 pLKO-GFP (n = 9) and EPHA10 sh3 tumors (n = 7). Left: Representative fields of IHC stained sections. Scale bars, 20 μm. Right: The percentages of Ki-67-positive cells per field were calculated for each group. Error bars represent SE; *p < 0.05; ***p < 0.001.