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Fig. 6 | Genome Biology

Fig. 6

From: The aspirin-induced long non-coding RNA OLA1P2 blocks phosphorylated STAT3 homodimer formation

Fig. 6

OLA1P2 mediated the aspirin-induced anti-metastatic phenotype and were associated with lower overall survival in CRC. a Stable OLA1P2-silencing COLO205 cells were injected into the immunodeficient mice, which were evaluated to determine the lung colonization capacity in tail vein assays. The bar graph represents 72 h time point measurements of the normalized photon flux for the animals. Representative images are shown; n = 6 for each group. b Number of metastases in the lungs of mice 4 weeks after tail vein injection; mean nodules per lung values are shown (bottom). Representative H&E staining of metastatic lung tumor tissues are shown (top). c Increased levels of OLA1P2 in clinical CRC tissues obtained from patients with regular use of aspirin were determined by qRT-PCR. d Immunoblotting analysis determined the protein levels of FOXD3 and phosphorylated STAT3 (Tyr705) in nuclear extract of clinical CRC samples obtained from patients with or without regular use of aspirin. e Linear regression analysis revealed the inverse correlation between FOXD3 and phosphorylated STAT3 (Tyr705) protein levels in nuclear extract of CRC tissues obtained from patients with regular use of aspirin (n = 46). f Lower OLA1P2 levels were correlated with increased pathological grade of CRC. g The curves show the lower overall survival of CRC patients with low OLA1P2 levels compared with CRC patients with high OLA1P2 levels. h A model illustrating the putative roles of aspirin-induced OLA1P2 in controlling the formation of phosphorylated STAT3 homodimers. *: P <0.05; **: P <0.01; ***: P <0.001

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