Figure 4
From: miR-96 promotes cell proliferation, migration and invasion by targeting PTPN9 in breast cancer
PTPN9 was predicted as a target of miR-96 and was downregulated in breast cancer tissues.
(A) Schematic description of the hypothesized duplex formed by interaction between the PTPN9 3′-UTR binding site and miR-96. The predicted free energy value of the hybrid is indicated. The seed recognition site is denoted, and all nucleotides in this region are highly conserved across species, including human, mouse and rat. (B and C) Western blotting analysis of the expression levels of PTPN9 protein in 10 pairs of breast cancer tissues and matched adjacent noncancerous tissues. (B) Representative image; (C) quantitative analysis. (D) Quantitative RT-PCR analysis of the relative expression levels of PTPN9 mRNA in 10 pairs of breast cancer tissues and matched adjacent noncancerous tissues. (E) Pearson’s correlation scatter plot of the fold-change of miR-96 and PTPN9 protein in human breast cancer tissues. (F) Pearson’s correlation scatter plot of the fold change of miR-96 and PTPN9 mRNA in human breast cancer tissues. (G–I) MCF-7 cells were infected with a control lentivirus (pre-miR-NC-LV) or a lentivirus to overexpress miR-96 (pre-miR-96-LV) and then implanted subcutaneously into 4-week-old nude mice. Tumor growth was evaluated at day 21 after cell implantation. Mice implanted with wide-type MCF-7 cells (Mock) serve as the negative control. (G) Western blotting analysis of PTPN9 protein levels in the tumors from implanted mice. (H) Quantitative RT-PCR analysis of PTPN9 mRNA levels in the tumors from implanted mice. (I) Immunohistochemical analysis of PTPN9 protein levels in the tumors from implanted mice. *P < 0.05; **P < 0.01; ***P < 0.001.
