Fig. 1: EphA7 demethylation via the dCas9-Tet1 system inhibited CC progression and induced apoptosis. | Cell Death & Disease

Fig. 1: EphA7 demethylation via the dCas9-Tet1 system inhibited CC progression and induced apoptosis.

From: Targeted demethylation of the EphA7 promoter inhibits tumorigenesis via the SP1/DNMT1 and PI3K/AKT axes and improves the response to multiple therapies in cervical cancer

Fig. 1

A Western blotting was performed and revealed that EphA7 expression was upregulated in the dCas9-Tet1 with act-sgRNAs group (demethylation) compared with the dCas9-Tet1 group (control) in both CaSki and SiHa cells (n = 3). B Compared with the control, targeted demethylation of EphA7 effectively inhibited the proliferation of CaSki and SiHa cells, as determined via the MTT assay (P < 0.05) (n = 6). C Transwell assays revealed that EphA7 demethylation (n = 6) strongly reduced the number of migrated CC cells compared with that in the control group (P < 0.05). D The epithelial marker CDH1 (E-cadherin) was upregulated due to the demethylation of EphA7 (n = 3), whereas the mesenchymal markers CDH2 (N-cadherin) and Snail1 were downregulated in CaSki and SiHa cells. E Western blotting was used to verify that the demethylation of EphA7 increased the expression of Bax, downregulated the expression of Bcl-2 and promoted caspase-3 activity (P < 0.05) in CaSki and SiHa cells (n = 3). Error bars represent the means ± SDs, P values were calculated using two-tailed unpaired Student’s t tests (A–E). *P < 0.05, **P < 0.01, ***P < 0.001.

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