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. Author manuscript; available in PMC: 2016 May 18.
Published in final edited form as: Oncogene. 2015 Mar 9;34(49):5997–6006. doi: 10.1038/onc.2015.48

Figure 1. miR-200c decelerates tumor growth.

Figure 1

(A) RFP was induced in tumors after DOX administration, as seen by FACS analysis and fluorescent microscopy. Scale bar represents 5mm. (B) miR-200c was induced to a physiological level, compared with its levels in different subtypes of p53null tumors (20), as shown by qPCR. (C) Tumor growth, as measured by the daily increase in tumor volume, was significantly lower in the DOX-treated group compared with untreated controls. (D) Tumor weight at the end of the treatment showed that the miR-200c-expressing tumors were much smaller than untreated controls. (E) The Ki67 proliferation marker was significantly decreased in miR-200c-induced tumors, revealing that the tumor growth deceleration was due, in part, to a lower proliferation rate. Scale bar represents 50μm. (F) Tumor latency increased with miR-200c upregulation. Equal numbers (5 000) of GFP+ and RFP+ cells were injected into the cleared fat pads of wild-type Balb/c recipient mice, and tumors were palpated every day to establish their latency, while maintaining vehicle or DOX treatment.