SELENBP1 inhibits progression of colorectal cancer by suppressing epithelial-mesenchymal transition.

Selenium-binding protein 1 (SELENBP1) is frequently dysregulated in various malignancies including colorectal cancer (CRC); however, its roles in progression of CRCs and the underlying mechanism remain to be elucidated. In this study, we compared the expression of SELENBP1 between CRCs and colorectal normal tissues (NTs), as well as between primary and metastatic CRCs; we determined the association between SELENBP1 expression and CRC patient prognoses; we conducted both in vitro and in vivo experiments to explore the functional roles of SELENBP1 in CRC progression; and we characterized the potential underlying mechanisms associated with SELENBP1 activities. We found that the expression of SELENBP1 was significantly and consistently decreased in CRCs than that in adjacent NTs, while significantly and frequently decreased in metastatic than primary CRCs. High expression of SELENBP1 was an independent predictor of favorable prognoses in CRC patients. Overexpression of SELENBP1 suppressed, while silencing of SELENBP1 promoted cell proliferation, migration and invasion, and in vivo tumorigenesis of CRC. Mechanically, SELENBP1 may suppress CRC progression by inhibiting the epithelial-mesenchymal transition.

Security enhancement mechanism based on contextual authentication and role analysis for 2G-RFID systems.

The traditional Radio Frequency Identification (RFID) system, in which the information maintained in tags is passive and static, has no intelligent decision-making ability to suit application and environment dynamics. The Second-Generation RFID (2G-RFID) system, referred as 2G-RFID-sys, is an evolution of the traditional RFID system to ensure better quality of service in future networks. Due to the openness of the active mobile codes in the 2G-RFID system, the realization of conveying intelligence brings a critical issue: how can we make sure the backend system will interpret and execute mobile codes in the right way without misuse so as to avoid malicious attacks? To address this issue, this paper expands the concept of Role-Based Access Control (RBAC) by introducing context-aware computing, and then designs a secure middleware for backend systems, named Two-Level Security Enhancement Mechanism or 2L-SEM, in order to ensure the usability and validity of the mobile code through contextual authentication and role analysis. According to the given contextual restrictions, 2L-SEM can filtrate the illegal and invalid mobile codes contained in tags. Finally, a reference architecture and its typical application are given to illustrate the implementation of 2L-SEM in a 2G-RFID system, along with the simulation results to evaluate how the proposed mechanism can guarantee secure execution of mobile codes for the system.

GJA1 promotes hepatocellular carcinoma progression by mediating TGF-ß-induced activation and the epithelial-mesenchymal transition of hepatic stellate cells.

INTRODUCTION: Gap junction protein, alpha 1 (GJA1), which is correlated with recurrences and unfavorable prognoses in hepatocellular carcinomas (HCCs), is one of the specific proteins expressed by activated hepatic stellate cells (HSCs). METHODS: Expression of GJA1 was compared between HCCs and nontumor tissues (NTs), between hepatic cirrhosis and NTs, and between primary and metastatic HCCs using transcriptomic datasets from the Gene Expression Omnibus and the Integrative Molecular Database of Hepatocellular Carcinoma. The in vitro activities of GJA1 were investigated in cultured HSCs and HCC cells. The underlying mechanism was characterized using Gene Set Enrichment Analysis and validated by western blotting. RESULTS: The expression of GJA1 was significantly increased in HCCs and hepatic cirrhosis compared to that in NTs. GJA1 was also overexpressed in pulmonary metastases from HCCs when compared with HCCs without metastasis. Overexpression of GJA1 promoted while knockdown of GJA1 inhibited proliferation and transforming growth factor (TGF)-ß-mediated activation and migration of cultured HSCs. Overexpression of GJA1 by lentivirus infection promoted proliferation and migration, while conditioned medium from HSCs overexpressing GJA1 promoted migration but inhibited proliferation of Hep3B and PLC-PRF-5 cells. Lentivirus infection with shGJA1 or conditioned medium from shGJA1-infected HSCs inhibited the proliferation and migration of HCCLM3 cells that had a high propensity toward lung metastasis. Mechanistically, GJA1 induced the epithelial-mesenchymal transition (EMT) in HSCs and HCCLM3 cells. CONCLUSION: GJA1 promoted HCC progression by inducing HSC activation and the EMT in HSCs. GJA1 is potentially regulated by TGF-ß and thus may be a therapeutic target to inhibit HCC progression.