Figure 5.

Aberrant splicing of TEAD2 is responsible for PHF5A-promoted CRC proliferation and migration

(A) CCK8 assays of HCT-8 cells stably overexpressing PHF5A or control treated with pladienolide B (PB) (2 nM) (n = 3). (B) Wound-healing and (C) transwell assays of HCT-8 cells stably overexpressing PHF5A or control treated with PB (1 nM) (n = 3). Scale bar, 20 μm. (D) Inclusion of TEAD2 exon 2 was examined by RT-PCR in HCT8 cells stably overexpressing PHF5A upon PB treatment (n = 3). (E) Protein levels of TEAD2-L and TEAD2-S in PHF5A overexpressing CRC cells upon PB treatment. (F) Immunoblotting analysis of TEAD2 protein level in cells transfected with specific siRNAs targeting TEAD2 exon 2 inclusion isoform (TEAD2-L). HCT-8 cells stably overexpressing PHF5A were transfected with siTEAD2-L or siNC, and subjected to (G) CCK8, (H) wound-healing, and (I) transwell assays. Scale bar, 20 μm. Experiments were repeated at least three times. Data are expressed as mean ± SD.