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Fig. 5 | Molecular Cancer

Fig. 5

From: Reciprocal activation between STAT3 and miR-181b regulates the proliferation of esophageal cancer stem-like cells via the CYLD pathway

Fig. 5

Reciprocal interaction between STAT3 and miR-181b conferred resistance to apoptosis. a Flow cytometry apoptosis analysis of SFCs treated with p-STAT3 inhibitor JSI-124 and miR-181b inhibitor. b Apoptosis analysis of SFCs treated with JSI-124 and miR-181b mimic by flow cytometry. SFCs were transiently transfected with miR-181b mimic and treated with 10 μM JSI-124. c Western blot analysis of SFCs treated with JSI-124 and miR-181b mimic. β-Actin served as an internal control. d Flow cytometry to determine apoptosis of SFCs treated with miR-181b inhibitor and vector pcDNA3.1 STAT3. SFCs were dissociated with trypsin, transiently transfected with vector pcDNA3.1 STAT3, and treated with 10 μM JSI-124 for 4 h. e qPCR analysis of miR-181b in SFCs treated with miR-181b inhibitor and pcDNA3.1 STAT3 vector. U6 snRNA served as an internal control. Error bars represent mean ± SD

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Molecular Cancer

ISSN: 1476-4598