We identified an inadvertent error in Figure 4J, where the band for ERK1/2 (T202/T204) and the corresponding α-tubulin loading control were mistakenly used from an image at a similar position from another experimental group due to the high similarity between the bands during figure preparation. This error does not affect the overall conclusion of the study, but we believe it is very important to correct it for accuracy and clarity. We sincerely apologize for this oversight and any confusion it may have caused. The corrected Figure 4 is shown below.
Figure 4.
E2F1 expression was regulated by miR-1205 via direct CDS binding and indirect KRAS signaling inhibition. A. E2F1 protein levels in A549 and H460 cells after transfected with siE2F1 or NC for 72 h, 10 nM. B. MTT analysis of A549 and H460 cells transfected with miR-1205 mimics or siE2F1 or NC for 72 h, 10 nM. C and D. QRT-PCR and WB analysis of E2F1 mRNA and protein levels in A549 and H460 cells after transfected with miR-1205. E. Predicted binding between miR-1205 and matched sequence in the CDS of E2F1. Mutant sequence of miR-1205 (mut miR-1205) and E2F1 CDS (mut E2F1 CDS with mut A and mut B) were shown. F. Luciferase activity in cells transfected with miR-1205 and reporter plasmids containing wt or mut E2F1 CDS. G. Luciferase activity in cells transfected with miR-1205 or mut miR-1205 and reporter plasmids containing wt E2F1 CDS. H. E2F1 protein level in miR-1205 deleted A549 cells by CRISPR/CAS9. I. A549 or H460 cells were transfected with different dose of siKRAS (5, 10 nM) or NC for 72 h, KRAS signaling and E2F1 protein level were analyzed. J. A549 or H460 cells were treated with SCH772984 (0, 0.1, 1, 10 μM) for 24 h, and analyzed for the expression of p-ERK1/2 and E2F1. Data are presented as the mean ± SEM of three independent experiments (* or #P<0.05, ** or ##P<0.01, *** or ###P<0.001).