Knockdown of 14-3-3zeta enhances radiosensitivity and radio-induced apoptosis in CD133+ liver cancer stem cells

14-3-3zeta is related to many cancer survival cellular processes. In a previous study, we showed that silencing 14-3-3zeta decreases the resistance of hepatocellular carcinoma (HCC) to chemotherapy. In this study, we investigated whether silencing 14-3-3zeta affects the radioresistance of cancer stem-like cells (CSCs) in HCC. Knockdown of 14-3-3zeta decreased cell viability and the number of spheres by reducing radioresistance in CSCs after gamma-irradiation (IR). Furthermore, the levels of pro-apoptotic proteins were upregulated in CSCs via silencing 14-3-3zeta after IR. These results suggest that 14-3-3zeta knockdown enhances radio-induced apoptosis by reducing radioresistance in liver CSCs.

Phosphorylation of 14-3-3zeta at serine 58 and neurodegeneration following kainic acid-induced excitotoxicity / 대한해부학회지

Oxidative stress-induced cell death leads to phosphorylation of 14-3-3zeta at serine 58. 14-3-3zeta is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3zeta phosphorylation in the hippocampus and amygdala of mice after KA treatment. Mice were killed at 2, 6, 24, or 48 h after KA (30 mg/kg) injection. We observed an increase in TUNEL and Fluoro-Jade B (FJB)-stained neurons in the hippocampus and amygdala of KA-treated mice. Phospho (p)-14-3-3zeta and p-JNK expression was increased in the hippocampus 2 and 6 h after KA treatment, respectively. In immunohistochemical analysis, p-14-3-3zeta-positive cells were present in the CA3 region of the hippocampus and the central nucleus of amygdala (CeA) of KA-treated mice. Thus, phosphorylation of 14-3-3zeta at serine 58 may play an important role in KA-induced hippocampal and amygdaloid neuronal damage.

Immunohistochemical study of 14-3-3-sigma and -zeta in ovarian cancer / 부인종양

OBJECTIVE: To evaluate the expression level, localization and distribution of 14-3-3sigma and zeta proteins in human ovarian epithelial carcinoma cells. METHODS: Epithelial carcinoma, benign epithelial tumor and normal ovarian tissues were evaluated by immunohistochemistry. For this study, mucinous adenoma (n=10), serous adenoma (n=10), mucinous adenocarcinoma (n=10) and serous adenocarcinoma (n=10) of ovary and normal ovarian tissue (n=10) were analyzed. Goat anti 14-3-3sigma polyclonal antibody and rabbit anti-14-3-3zeta polyclonal antibody were used as primary antibodies. RESULTS: The 14-3-3sigma protein expression in the glandular epithelium was not statistically different among normal ovary, cystadenoma and cystadenocarcinoma. The 14-3-3zeta protein expression in the glandular epithelium was significantly higher for cystadenocarcinoma than for cystadenoma and normal ovary. The 14-3-3sigma and zeta proteins were immunohistochemically demonstrated in the nuclei and more preferably in the cytoplasm of adenocarcinoma epithelial cells. CONCLUSION: The expression of 14-3-3zeta protein increased significantly in ovarian adenocarcinoma compared with adenoma and normal ovary. It is suggested that 14-3-3zeta protein expression may play an important role in abnormal growth of ovarian epithelial tumor cell.