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. 2014 Sep 3;105(9):1152–1159. doi: 10.1111/cas.12479

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© 2014 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Fig 1 — SS18-SSX-regulated miR-17 promotes colony formation ability in synovial sarcoma cells. (a) Schematic diagram identifying microRNA to cause marked tumor growth on synovial sarcoma cells. (b) Fuji cells infected with the OncomiR miRNA Precursor Virus Library formed large colonies in soft agar. (c) Total RNA was isolated from the largest two colonies formed by Fuji cells (b), and subjected to semi-quantitative RT-PCR using the OncomiR miRNA Precursor Virus Library, followed by sequencing. (d) Diagram of a polycistronic microRNA cluster termed miR-17-92. Sequence of miR-17-5p is shown. (e) Endogenous expression levels of miR-17 in indicated samples were examined by semi-quantitative RT-PCR. RNU6B was used as an internal control for evaluating microRNA expression. (f) mir-17 expression levels were examined by quantitative RT-PCR in Fuji cells with enforced expression of SS18-SSX2 (f), with SS18-SSX depletion (g), and in indicated cell lines and clinical samples (h). *P < 0.05 versus control cells.