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IHC was performed in 45 HCC tissues samples according to the methods that had been used in previous studies [29]. All statistical analyses were performed using SPSS13.0 for Windows (SPSS Inc., Chicago, IL, U.S.). P?S1PR1 respectively) ( Fig. 1A). Among the 83 patients with primary HCC, 51 (61.45%) showed a reduction in the miR-219-5p level of over 50% relative Protein Tyrosine Kinase inhibitor to their matched non-tumor adjacent tissues ( Fig. 1B). We then studied the correlation between miR-219-5p expression and the clinicopathological characteristics of HCC. The patients with lower levels of miR-219-5p expression tended to have larger tumor sizes (?5?cm; P?=?0.027) and poor differentiation (P?=?0.030; Table 1). Kaplan�CMeier analysis also showed that downregulation of miR-219-5p was associated with decreased survival ( Fig. 1C). Specifically, the median overall survival time was 13.0 and 30.0?months in miR-219-5p downregulation and normal/upregulation groups, respectively (P?=?0.005, log-rank test). We also found that, compared to normal liver cell line HL-7702, miR-219-5p was downregulated in all HCC cell lines: (Huh-7, 0.06?��?0.02-fold; MHCC-97H, 0.57?��?0.12-fold; MHCC-97L, Tofacitinib chemical structure 0.74?��?0.07-fold; HepG2, 0.11?��?0.02-fold; HCCLM6, 0.14?��?0.02-fold; Fig. 1D). The downregulated miR-219-5p in HCC prompted us to investigate whether miR-219-5p functions as a tumor suppressor. In HCC cell lines Huh-7 and HepG2, we found miR-219-5p expression was markedly decreased (Fig. 1C), and restoration of miR-219-5p expression by miR-219-5p mimics inhibited cell proliferation in Huh-7 and HepG2 cells (Fig. S1A and Fig. 2A). To provide further evidence that miR-219-5p is involved in HCC cell growth, we selected the HCC cell line MHCC-97L, which has a relatively high level of miR-219-5p (Fig. 1C), and studied the effects of an inhibitor of miR-219-5p. In contrast, proliferation of MHCC-97L cells transfected with miR-219-5p inhibitors was found to be higher than that of the cells transfected with i-NCs (Fig. S1B and Fig. 2B). Colony formation assay showed that enforced expression of miR-219-5p resulted in a decrease of more than 20% in the number of colonies in HepG2 cells (Fig. 2C). Transfection of miR-219-5p inhibitors into MHCC-97L cells significantly increased the number of colonies when relative to i-NCs (Fig. 2D).