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. 2020 Jan 23;7(5):1903035. doi: 10.1002/advs.201903035

Figure 3.

Figure 3

miR‐135a upregulated Nanog expression and enhanced CSC capacity of tumor cells in vivo. A) Expression of miR‐135a (left panel) and the DNMT1 protein (right panel) in Huh7 cells without (WT, wild‐type) or with miR‐135a knockdown (miR‐35a KD) assessed by qRT‐PCR or WB in triplicate. B) Expression of Nanog in Huh7 cells without (WT) or with miR‐135a knockdown (miR‐35a KD) assessed by qRT‐PCR and WB in triplicate. C) Expression of Nanog assessed by qRT‐PCR and WB and D) Nanog+ cell rate assessed by FACS analysis in tumors derived from tumor cells without (WT) or with miR‐135a knockdown (miR‐135a KD). n = 5 in WT, n = 4 in miR‐135a KD. E) Representative image (left panel) and tumor growth curve (right panel) of tumors derived from tumor cells with (miR‐135a KD) or without (WT) miR‐135a knockdown in mice, n = 5 each group. F) Expression of Nanog assessed by qRT‐PCR and WB and G) the Nanog+ cell rate was assessed by FACS analysis in tumors with (Len‐miR‐135a) or without (Len‐NC) miR‐135a upregulation, n = 5 each group. H) Representative image (left panel) and growth curve (right panel) of tumors with with (Len‐miR‐135a) or without (Len‐NC) miR‐135a upregulation in mice, n = 5 each group. The image of GAPDH from WB in (A) was also used in (B). Representative data are shown as the mean ± SD. P value was assessed by Student's t test.