Wu Y.,Nanyang City Central Hospital |
Zhang J.,Xinxiang Medical University |
Zhang H.,Nanyang City Central Hospital |
Zhai Y.,Nanyang City Central Hospital
Oncology Letters | Year: 2016
Hepatitis B virus (HBV) X protein (HBx) is implicated in the development of hepatocellular carcinoma (HCC). Yes-associated protein 1 (YAP) is an important protooncogene, which is a downstream effector molecule in the Hippo signaling pathway. The aim of the present study was to investigate the association between HBx expression in HCC samples and YAP expression in the Hippo pathway. A total of 20 pathologically confirmed HCC samples, 20 corresponding adjacent non-tumor liver tissues and 5 normal liver tissue samples were collected. The expression of HBx and YAP in the tissues was analyzed by quantitative reverse transcription-polymerase chain reaction and western blot analysis. The intensity and location of YAP expression were analyzed by immunohistochemistry. YAP mRNA and protein expression levels in HCC samples infected with HBV were significantly higher than those of normal liver tissues. Furthermore, YAP expression was positively correlated with HBx expression in HBV-positive HCC samples. Immunohistochemical staining revealed that YAP was predominantly expressed in the nuclei in HBV-positive HCC tissues. YAP expression was significantly decreased in the normal liver tissue and corresponding adjacent liver tissue when compared with the HCC tissues and by contrast to HCC tissues, YAP was predominantly located in the cytoplasm. In conclusion, these results indicate that the YAP gene is a key driver of HBx-induced liver cancer. Therefore, YAP may present a novel target in the treatment of HBV-associated HCC. © 2016, Spandidos Publications. All rights reserved.
Tao H.-Y.,Nanyang City Central Hospital |
Qu Z.-Y.,Nanyang City Central Hospital |
Wei G.-M.,Nanyang City Central Hospital |
Sheng J.,Nanyang City Central Hospital |
And 2 more authors.
World Chinese Journal of Digestology | Year: 2016
AIM: To explore the role of LKB1 in gastric cancer cells and the related mechanism. METHODS: Real-time PCR and Western blot were used to detect the expression of LKB1 in SGC7901 cells carrying LKB1 expression vector or siRNA against LKB1. Flow cytometry was used to detect the apoptosis of SGC7901 cells after LKB1 overexpression or knockdown. Reactive oxygen detection kits were applied to detect the impact of LKB1 on ROS production. MTT method was used to determine intracellular ROS production after NAC inhibition. Western blot was used to detect the expression of apoptosis related proteins in SGC7901 cells after LKB1 overexpression or knockdown. RESULTS: LKB1 expression was efficiently enhanced or silenced by LKB1 expression vector or siRNA against LKB1, respectively. The number of SGC7901 cells decreased as its proliferation rate decreased and apoptosis rate increased (3.54% vs 1.29%). Intracellular ROS production was increased but blunted by the use of NAC. The apoptosis of SGC7901 cells was significantly reduced following the inhibition of intracellular ROS, but the siRNA transfected group exhibited an opposite trend. Western blot analysis showed that LKB1 overexpression up-regulated the expression of cleaved Caspase3 in SGC7901 cells significantly (about 3.12 times), compared with control cells, but the expression of cleaved Caspase3 in the siRNA transfected group was decreased. CONCLUSION: LKB1 raises the production of ROS and up-regulates the expression of cleaved Caspase3 to promote gastric cancer cell apoptosis. Hence, LKB1 plays an important role in the development of gastric cancer and it may be a valuable target for chemotherapy of gastric cancer. © 2016 Baishideng Publishing Group Inc. All rights reserved.