Regulatory role of CDX2 and NOX4 expression associated with recurrent nasopharyngeal carcinoma.

OBJECTIVE: Nasopharyngeal carcinoma (NPC) is a malignancy caused by Epstein-Barr virus (EBV). NPC is radiosensitive and has a high frequency of treatment failure due to metastasis, which results in recurrent nasopharyngeal carcinoma (rNPC). PATIENTS AND METHODS: In the present study, nasopharyngeal carcinoma biopsies were obtained from NPC and rNPC patients, as well as healthy controls, and reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, and immunoblotting analyses were performed. RESULTS: The RTPCR data showed expression of CDX2 and NOX4 in rNPC biopsy samples but not in control or NPC samples. Immunohistochemical and immunoblotting analyses confirmed the expression of CDX2 and NOX4 in rNPC samples, but not in NPC biopsy samples. CONCLUSIONS: The finding concludes that an association of CDX2 and NOX4 expression with rNPC was noted; thus, these proteins may have value as prognostic indicators and may facilitate the development of novel therapeutics for rNPC patients.

L-3-n-Butylphthalide protects rats' cardiomyocytes from ischaemia/reperfusion-induced apoptosis by affecting the mitochondrial apoptosis pathway.

AIMS: This study investigated the role of L-3-n-Butylphthalide (NBP) in cardiac protection. METHODS: The left anterior descending coronary arteries (LAD) of the rats were occluded for 30 min following by 2-h reperfusion to make the ischaemia/reperfusion models. Neonatal cardiomyocytes were cultured and subjected to hypoxia. L-3-n-Butylphthalide was administered intraperitoneally 2 h before the surgery and right after the reperfusion in the in vivo experiments or added to the culture medium in vitro. Haemodynamic parameters were recorded to evaluate the cardiac functions, triphenyltetrazolium chloride (TTC) and Evens blue staining were used to determine the area of risk and infarct area, apoptotic cell numbers were counted with terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining. Western blotting was used to determine the apoptotic protein levels and immune staining to determine the translocation of Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein. RESULTS: Our research showed for the first time that L-3-n-Butylphthalide had great effects in improving cardiac hemodynamic function and decreasing cardiac infarct areas and apoptotic cell numbers in the peri-infarct areas. The apoptotic signals investigation showed that L-3-n-Butylphthalide affected the mitochondrial pathway including Bcl-2 protein expression, inhibition of caspase 3 activation and cytochrome C releasing. Besides, Glyceraldehyde-3-phosphate dehydrogenase protein translocation was inhibited by L-3-n-Butylphthalide treatment, and this effect was mediated by endogenous reactive oxygen species (ROS). CONCLUSION: L-3-n-Butylphthalide protects cardiomyocytes from ischaemia/reperfusion-induced apoptosis by antioxidant effect and affecting mitochondrial apoptotic pathway.