Figure 4.
The influence of TP73‐AS1 upregulation on the role of miR‐125a in breast cancer cell malignancy in vitro. (a) RT‐qPCR determined the transfection efficiency of miR‐125a and miR‐control in HCC‐70 and MB231 cells. (
) miR‐control and (
) miR‐125a. (b–f) HCC‐70 and MB231 cells were transfected with miR‐125a or miR‐control, and cotransfected with miR‐125a and either TP73‐AS1 or vector. (b) CCK‐8 determined cell proliferative capacity after transfection at 0 hour, 24 hours, 48 hours and 72 hours. HCC‐70 (
) miR‐control, (
) miR‐125a, (
) miR‐125a+vector and (
) miR‐125a+TP73‐AS1. MB231 (
) miR‐control, (
) miR‐125a, (
) miR‐125a+vector and (
) miR‐125a+TP73‐AS1. (c) Flow cytometry examined apoptosis rate after transfection at 24 hours. (
) miR‐control, (
) miR‐125a, (
) miR‐125a+vector and (
) miR‐125a+TP73‐AS1. (d, e) Transwell assays were performed to evaluate cell migration and invasion abilities at 24 hours. (
) miR‐control, (
) miR‐125a, (
) miR‐125a+vector and (
) miR‐125a+TP73‐AS1. (f, g) Western blotting tested protein expression of Ki67, cleaved caspase‐3, N‐cadherin and Vimentin after transfection at 24 hours. (f) HCC‐70 (
) miR‐control, (
) miR‐125a, (
) miR‐125a+vector and (
) miR‐125a+TP73‐AS1. (g) MB231 (
) miR‐control, (
) miR‐125a, (
) miR‐125a+vector and (
) miR‐125a+TP73‐AS1. Data represent mean ± SEM and *P < 0.05.