Daqing Zhao

ATRA-inhibited proliferation in glioma cells is associated with subcellular redistribution of β-catenin via up-regulation of Axin

Retinoic acid (RA) is a major chemopreventive agent which exerts strong anti-tumor activity partly by trans-repressing the Wnt/β-catenin signaling pathway in some tumor cell lines. However, the definite mechanism of RA trans-repression of the Wnt/β-catenin signaling pathway has not been elucidated clearly. In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of β-catenin. Transfecting C6 cells with rAxin further confirmed that increased expression of Axin is obligate for inhibition of proliferation and the increase of the cytoplasmic β-catenin. Our results suggested that Axin might play an important role in RA-mediated anti-proliferative effects of glioma cell lines.

CIDE-3 interacts with lipopolysaccharide-induced tumor necrosis factor, and overexpression increases apoptosis in hepatocellular carcinoma

Abstract Cell death–inducing DFF45-like effector-3 (CIDE-3) is a novel member of an apoptosis-inducing protein family, but its function is unknown. CIDE-3 shows a different distribution pattern in hepatocellular carcinoma (HCC) tissues and normal adjacent tissues. Therefore, this work tested the hypothesis that CIDE-3 induces apoptosis in HCC cells, inhibiting oncogenesis and tumor development. We used immunohistochemistry to evaluate the expression of CIDE-3 in 82 HCC samples and 51 adjacent liver tissues. Overexpression of CIDE-3 induced apoptosis, as detected by flow cytometry, in the HCC cell line SMMC-7721, which had undetectable levels of CIDE-3 in the absence of CIDE-3 overexpression. A yeast two-hybrid system was employed to screen for proteins that interact with CIDE-3. The expression of CIDE-3 was decreased in HCC tissue, compared to adjacent normal tissues, and CIDE-3 expression and HCC differentiation were positively correlated. CIDE-3 expression levels were lower in poorly differentiated HCC tissue than in well-differentiated HCC tissue. Overexpressed CIDE-3 inhibited proliferation and induced apoptosis in HCC cells. We found that lipopolysaccharide-induced tumor necrosis factor (LITAF) interacted with CIDE-3 in hepatic cells. This is the first demonstrated interaction between CIDE-3 and LITAF, and the first report that CIDE-3 induces apoptosis in hepatocellular carcinoma.