Fig. 3: METTL14 promotes the 5-FU-induced apoptosis. | Cell Death & Disease

Fig. 3: METTL14 promotes the 5-FU-induced apoptosis.

From: METTL14-dependent maturation of pri-miR-17 regulates mitochondrial homeostasis and induces chemoresistance in colorectal cancer

Fig. 3

A Overexpression and knockdown efficiency of METTL14 in HCT116 cells. B The 5-FU IC50 of HCT116 cells in different groups. C EdU proliferation assay of HCT116 cells with different METTL14 expression levels after 5-FU treatment. P (NC vs. METTL14 OE) = 0.0265; P (si-NC vs. si-METTL14) = 0.0379. D Annexin V-PE/7AAD apoptosis assay of HCT116 cells with different METTL14 expression levels after 5-FU treatment. P (NC vs. METTL14 OE) = 0.0095; P (si-NC vs. si-METTL14) = 0.0005. E Western blot analysis of PARP, Cleaved PARP, Caspase7, Cleaved Caspase7, BCL2 and BAX protein expression levels in different METTL14 expression levels HCT116 cells treated with 5-FU. F Knockdown efficiency of stably transfected METTL14 CRC cells. G Nude mice were implanted with tumor cells subcutaneously. H Tumor sizes and weights of xenograft after 6 times 5-FU treatment. P = 0.0360. I The changes of tumors volume during the treatment of 5-FU. J H&E and immunohistochemistry analysis of Caspase7 levels in two groups. P = 0.0077. Results shown were representative of at least 3 independent experiments. Statistical significance in (B-D), (H), (J) was assessed by student’s t-test. *, P<0.05; **, P<0.01; ***, P<0.001. Error bars, SD. Scale bars, 400 μm in (C), 100 μm in (J). The IHC score and grey value of protein bands has been quantified by Image J.

Back to article page