BACKGROUNDThe conformation of a subset of phosphorylated serines or threonines preceding proline motifs is regulated by the prolyl isomerase Pin1. Pin1 plays a critical role in oncogenesis. The aim of this study is to explore the relationship between the expression of Pin1 and clinicopathological factors in squamous cell carcinoma and adenocarcinoma of the lung, and to analyze the correlation between Pin1 and β-catenin.

METHODSThe expression of Pin1 and β-catenin proteins was detected in 69 lung cancer cases by immunohistochemical SP method, and in 30 fresh lung samples by Western blot.

RESULTSImmunohistochemically, the overexpression of Pin1 and β-catenin in lung cancer was 78.3% (54/69) and 63.8% (44/69), respectively. The expression of Pin1 and β-catenin was not related to age, sex, histological classification, differentiation, lymph node metastasis and pTNM stages. There was a positive correlation between overexpression of Pin1 and aberrant β-catenin expression (P < 0.05). Western blot results showed that the expression of Pin1 and β-catenin in lung cancer tissues was significantly higher than that of paracancerous lung tissues (P < 0.05).

CONCLUSIONSPin1 is overexpressed in squamous cell carcinoma and adenocarcinoma of the lung and may play a critical role in oncogenesis of lung cancer. Overexpression of Pin1 might contribute to the upregulation of β-catenin and it may be one of the pathways for Pin1 to work.

Background/Aims: This study aimed to investigate the biological function and regulatory mechanism of TCN1 in colorectal cancer (CRC). Methods: We studied the biological function of TCN1 by performing gain-of-function and loss-offunction analyses in HCT116 cell lines; examined the effects of TCN1 on the proliferation, apoptosis, and invasion of CRC cells; and determined potential molecular mechanisms using HCT116 and SW480 CRC lines and mouse xenotransplantation models. Tumor xenograft and colonization assays were performed to detect the tumorigenicity and metastatic foci of cells in vivo. Results: TCN1 knockdown attenuated CRC cell proliferation and invasion and promoted cell apoptosis. Overexpression of TCN1 yielded the opposite effects. In addition, TCN1-knockdown HCT116 cells failed to form metastatic foci in the peritoneum after intravenous injection. Molecular mechanism analyses showed that TCN1 interacted with integrin subunit β4 (ITGB4) to positively regulate the expression of ITGB4. TCN1 knockdown promoted the degradation of ITGB4 and increased the instability of ITGB4 and filamin A. Downregulation of ITGB4 at the protein level resulted in the disassociation of the ITGB4/plectin complex, leading to cytoskeletal damage. Conclusions TCN1 might play an oncogenic role in CRC by regulating the ITGB4 signaling pathway.

Aim To establishan inflammatory model of mouse monocyte macrophages ( RAW264. 7) using li-popolysaccharide (LPS), and to investigate the antiinflammatory activity and mechanism of tanshinone II-A (Tan IIA). Methods Cell viability was determined by CCK-8 method. Cell migration was detected by Tr-answell apparatus. TNF-α, IL-6, IL-1 p, MCP-1 content in cell supernatant was analyzed using ELISA method. The protein expression of MMP-2, MMP-9, TLR4, κB-α, p-κB-α, NFκB and p-NFκB in RAW264.7 cells was investigated by Western blot. Results Tan IIA significantly inhibited .the secretion of TNF-α, IL-6, IL-1β and MCP-1 in LPS induced RAW264.7 cell culture medium , and significantly down-regulated the expression of matrix metalloprotein-ase-2 (MMP-2), MMP-9, TLR4, p-κB-α and p-NFκB , inhibited IκB-α phosphorylation and NFκB entry into the nucleus and activation. Conclusion Tan IIA can inhibit the release of inflammatory factors through the regulation of TLR4/IκB-α/NFκB signaling pathway.