Fig. 5: METTL3 promoted breast cancer cell proliferation by mediating p21 expression.
From: Metformin exhibits antiproliferation activity in breast cancer via miR-483-3p/METTL3/m6A/p21 pathway
A, B Silencing of p21 inhibited the increasing of p21 induced by METTL3 knockdown in both RNA and protein level in SUM-1315 and MCF-7 cells. The relative RNA level was calculated by the 2−ΔΔCt method and normalized based on β-actin. The average mRNA level of p21 in the shNC group was set as 1. C–F Suppression of p21 alleviated the inhibitory effects on cell proliferation and colony formation mediated by METTL3. G IHC of subcutaneous xenograft tumors showed that a significant increase in the positive rate of Ki-67 while a significant decrease in the positive rate of p21 in the METTL3 overexpression group. H The protein level of METTL3 in the tumors of mice treated with metformin decreased than those with PBS, while the protein level of p21 increased in the metformin group. shNC, scramble control; shM3/shMETTL3-2, METTL3 knockdown; shM3 + siP21, METTL3 knockdown cells transfected with p21 siRNA; oeNC, negative control; oeNC-Met, oeNC-Met negative control group treated with metformin; oeMETTL3, METTL3 overexpression; oeMETTL3-Met, METTL3 overexpression group treated with metformin. Data represented the mean ± SD, *p < 0.05, **p < 0.01 vs. shMETTL3-2 group.
