miR106a Promotes the Growth of Transplanted Breast Cancer and Decreases the Sensitivity of Transplanted Tumors to Cisplatin
Authors You F, Li J, Zhang P, Zhang H, Cao X
Received 17 September 2019
Accepted for publication 7 December 2019
Published 13 January 2020 Volume 2020:12 Pages 233—246
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Eileen O'Reilly
Faping You, 1–5 Junhui Li, 1–4 Peijin Zhang, 1–4 Hui Zhang, 1–4 Xuchen Cao 1–4
1First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin 300060, People’s Republic of China; 2Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, People’s Republic of China; 3Tianjin’s Clinical Research Center for Cancer, Tianjin 300060, People’s Republic of China; 4Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Tianjin 300060, People’s Republic of China; 5Shengli Oilfield Central Hospital, Dongying, Shandong Province 257034, People’s Republic of China
Correspondence: Xuchen Cao
First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Huan-Hu-Xi Road, Hexi District 300060 Tel +86 22 23340123 2071
Email email@example.com, Tianjin, People’s Republic of China
Objective: To explore the effect of miR106a on the growth of breast cancer xenografts and the sensitivity of chemotherapeutic agents.
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.
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.
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.
Keywords: miR106a, breast cancer transplantation tumor, MDA-MB231, MCF7, chemotherapeutic drug sensitivity
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