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. 2019 May 15;11(5):2784–2800.

Figure 3.

Figure 3

Silencing FAT4 promoted EC proliferation, and overexpressing FAT4 suppressed EC proliferation. A: IC50 values of puromycin in HEC-1A, HEC-1B and RL95-2 cells. B: Knockdown (shFAT4) efficiency of FAT4 at the mRNA and protein levels in HEC-1A and HEC-1B cells. The data are presented mean ± SD, t-test, *P<0.05, **P<0.01. C: Efficiency of upregulating dCas9, FAT4 mRNA and FAT4 protein levels in RL95-2 cells. The data are presented as mean ± SD, t-test, ***P<0.001. D-F: Knockdown (shFAT4) of FAT4 in both the HEC-1B and HEC-1A cell lines significantly promoted EC cell proliferation compared with the negative (non-target) control (NC); upregulating (sgRNA) FAT4 in RL95-2 cells significantly inhibited EC cell proliferation compared with NC. The data are presented mean ± SD, t-test, *P<0.05, **P<0.01. G: EC cell colony formation was significantly increased by knockdown (shFAT4) of FAT4 in both HEC-1B and HEC-1A cells and significantly decreased upon upregulating (sgRNA) FAT4 in the RL95-2 cell line, The data are presented mean ± SD, t-test, *P<0.05, **P<0.01.