IHC-65 was found to be a potent inhibitor of platelet function . It inhibited platelet aggregation induced by threshold concentration of ADP, arachidonic acid and collagen with dose-dependent manner in vitro, and at 96?mol/L, AIR ( aggregation inhibition rate,) were 71.56, 66.93 and 68.47% respectively. IHC-65 inhibited platelet serotonin release induced by collagen,and at 96 ?mol/L, release inhibition rate was 82.97%. IHC-65 did not influence cAMP level in platelet significantly. It is concluded that IHC-65 inhibited platelet aggregation and its action mechanism may be related to inhibition of serotonin release and to antagonizing Ca ++ .

Objective This study is to explore the expression of CIP2A mRNA in hepatocellular carcinoma (HCC), and its correlations with clinicopathologic features and prognosis of HCC patients.Methods CIP2A mRNA expression was analyzed in four liver cancer cell lines (Hep-G2, MHCC97,SMMC-7721 and BEI-7402), one immortalized liver cell line L-O2, neoplastic tissues and adjacent matched non-neoplastic liver tissues in 120 HCC patients and normal liver tissues of 20 cases using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The correlations between CIP2A mRNA and clinicopathologic features and prognosis of HCC were analyzed. Results CIP2A mRNA was detected in Hep-G2, MHCC-97H, SMMC-7721 and BEL-7402, but not in L-O2.The positive rate of CIP2A mRNA expression was significantly increased in HCC tissues (78.3%)than in adjacent matched non-neoplastic liver tissues (28.3%) and normal liver tissues (5.0%,P＜0. 01). CIP2A mRNA expression was correlated with tumor size, differentiation and TNM stage (P＜0.05). Patients with positive expression of CIP2A mRNA had lower overall survival and diseasefree survival rates. Conclusions CIP2A mRNA, which is highly expressed in liver cancer cell lines and HCC tissues, may be involved in hepatocarcinogenesis. CIP2A mRNA may be a valuable biomarker for assessing the prognosis of HCC.

Purpose: Four and a half LIM protein 1 (FHL1) is involved in breast cancer (BC) development, but the regulatory mechanism involved remain unclear. In the present study, we examined the role of FHL1 in BC development. Methods: The expression of FHL1, miR-183-5p, and miR-96-5p in BC tissues was analyzed using StarBase analysis. FHL1 expression in BC tissues, a normal human breast epithelial cell line, and BC cell lines was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The relationship between FHL1 and miR-183-5p/miR-96-5p was analyzed via Pearson's rank correlation, TargetScan, and a dual-luciferase reporter assay. BT549 and MDA-MB-231 cells were transfected with either FHL1 and miR-183-5p mimics, or siFHL1 and a miR-183-5p inhibitor, respectively. The viability, colony number, migration, invasion, and tube length of BT549 and MDA-MB-231 cells were examined using cell counting kit-8, colony formation, wound-healing, Transwell, and tube formation assays, respectively. The levels of FHL1, vascular endothelial growth factor (VEGF), p53, E-cadherin, N-cadherin, and vimentin were quantified using western blotting and qRT-PCR. Results: FHL1 expression was downregulated in BC tissues and cells, whereas miR-183-5p and miR-96-5p were upregulated in BC tissues (negative correlation with FHL1 expression).FHL1 overexpression inhibited the viability, colony number, migration, and invasion of BC cells and the expression of VEGF, N-cadherin, and vimentin, and increased the expression of FHL1, p53, and E-cadherin in BT549 cells. Furthermore, a miR-183-5p mimic reversed these effects of FHL1 overexpression, whereas FHL1 silencing caused opposite results to those observed in MDA-MB-231 cells; however, this was reversed by a miR-183-5p inhibitor. Conclusion Our study suggests that miR-183-5p promotes cell proliferation, metastasis, and angiogenesis by negatively regulating FHL1 in BC.