Conclusion
Overexpression of miR106a can promote the growth of transplanted breast cancer and decrease the sensitivity of transplanted tumors to cisplatin. The mechanism may be related to abnormal activation of the Wnt-signaling pathway.
Methods
Breast cancer cell lines (MDA-MB231 and MCF7) were transfected with an miR106 mimic and miR106a inhibitor. BALB/c female nude mice were selected to construct a transplanted-tumor model. Cisplatin treatment was performed 2 weeks after inoculation. After 5 weeks, tumor tissue was weighed. Apoptosis of tumor cells was detected by TUNEL staining. The expression of these proteins (Ki67, β-catenin, cyclin D1 and cMyc) was detected by immunohistochemistry. The contents of P53, RUNX3, ABCG2, β-catenin, BAX, and BCL2 mRNA were detected by qRT-PCR.
Objective
To explore the effect of miR106a on the growth of breast cancer xenografts and the sensitivity of chemotherapeutic agents.
Results
The miR106a mimic (MM) group's tumor volume and weight were significantly bigger than those of the model group. miR106a mRNA content was higher than the blank control group, and β-catenin and Ki67 protein were strongly positive. β-catenin, BCL2, and ABCG2 mRNA content was were increased. P53, BAX, and RUNX3 mRNA content was decreased. The number of positive cells on TUNEL staining was significantly lower in the miR106a inhibitor (MI) group. After cisplatin treatment, inhibition of tumor growth was most obvious in the MI+DDP (cisplatin) group. Compared with the MM group, tumor growth in the MM+FH535 (Wnt-pathway inhibitor) group was significantly lower, and Wnt-pathway activity was decreased.