Fig. 3: miR-30c targeted and inversely regulated BCL9, thus repressing ecto-EEC migratory and invasive phenotypes. | Cell Death Discovery

Fig. 3: miR-30c targeted and inversely regulated BCL9, thus repressing ecto-EEC migratory and invasive phenotypes.

From: Endometrial epithelial cells-derived exosomes deliver microRNA-30c to block the BCL9/Wnt/CD44 signaling and inhibit cell invasion and migration in ovarian endometriosis

Fig. 3

A Online prediction of the binding site of BCL9 and miR-30c by TargetScan; B Dual-luciferase reporter gene assay to verify the binding of miR-30c to BCL9; C qRT-PCR measurement of the expression of miR-30c and BCL9 in ecto-EECs in response to the overexpression of miR-30c alone or in combination with BCL9; D Western blot measurement of the protein expression of BCL9 in ecto-EECs in response to the overexpression of miR-30c alone or in combination with BCL9; E Wound healing assay to detect the migration of ecto-EECs in response to the overexpression of miR-30c alone or in combination with BCL9; F Transwell assay to detect the invasion of ecto-EECs in response to the overexpression of miR-30c alone or in combination with BCL9. Cellular experiments were repeated three times. Measurement data were characterized as mean ± SD. The comparison between data of two groups was performed by independent sample t-test and that among multiple groups was performed with one-way ANOVA with Tukey’s post hoc test. *p < 0.05 versus the mimic-NC group, #p < 0.05 versus the miR-30c-mimic group.

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