The authors regret that in the original version of the manuscript, we accidently presented the wrong caspase-3 Western blots for MGC803 in the left panel of Fig. 2E. We also included an erroneous DAPI image in Fig. 3G (pENTER, BGC823). Both images were incorrectly incorporated during figure assembly. We have checked the original raw data and records of the experiments and the corrected figures are provided below. These corrections do not affect the results and conclusions of this article. The authors would like to apologise for any inconvenience caused.
Fig. 2.
miR-567 suppresses GC cell proliferation and increases drug sensitivity in vitro and in vivo. FACS assays (A) and EdU incorporation assays (B) of GC cells were performed after transfected with miR-567 mimic or anti-miR-567, Student's t-test, mean ± SD, *P<0.05; **P<0.01; *** P<0.001. (C&D) Dose-response curves of MGC803 and BGC823 treated with 5-FU for 36 h or oxaliplatin for 24 h, the cells were previously transfected with miR-NC, miR-567, anti-miR-NC or anti-miR-567. Parametric generalized linear model with random effects, Student's t-test, mean ± SD, *P<0.05; **P<0.01; *** P<0.001. (E) Western blot experiments were used to analyse the expression of c-casp3, casp3, c-PARP, PARP, c-casp9, casp9, p21, CDK4, CDK6 and CyclinD1 after miR-567 knockdown and overexpression in MGC803 and BGC823 cells. (F)In vivo image detection of the xenograft tumour growth. Growth curve was measured and drawn, *P<0.05. The tumour sections were under IHC staining using antibodies against Ki-67. Quantification of Ki67 staining of the xenograft tumours (right). ***P<0.001.
Fig. 3.
PIK3AP1 is the direct target of miR-567 and promotes GC cell proliferation and increases drug sensitivity. (A) Real-time PCR analysis were performed to detect the mRNA expression of candidate genes in MGC803 and BGC823 cells transfected with miR-567 mimic, Student's t-test, mean ± SD. (B) miR-567 and its putative binding sequences in the 3′UTR of PIK3AP1. A mutation was generated in the complementary site that bound to the seed region of miR-567. Luciferase reporter assay was used to determine miR-567 direct targeting the PIK3AP1 3′UTR, Student's t-test, mean ± SD, ***P<0.001. (B) Western blot analysis were performed to detect the protein expression of PIK3AP1 in MGC803 and BGC823 cells, both transfected with miR-567 mimic or anti-miR-567. CCK-8 assay (C), colony formation assay (D), FACS assays (E) and EdU incorporation assays (F) of GC cells were performed after transfected with PIK3AP1 or pENTER vector, Student's t-test, mean ± SD, *P < 0.05; **P < 0.01. (H) Western blot experiments were used to analyse the expression of pro-apoptosis proteins, cell cycle maker and related proteins in PI3K/AKT pathway after miR-567 knockdown and overexpression in MGC803 and BGC823 cells. (I) Dose-response curves of MGC803 and BGC823 treated with 5-FU for 36 h or oxaliplatin for 24 h, the cells were previously transfected with PIK3AP1 and pENTER. Parametric generalized linear model with random effects, Student's t-test, mean ± SD, *P<0.05; **P<0.01; *** P<0.001.