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ABSTRACT: To investigate the expression of SUMO-1 in human hepatocellular carcinoma (HCC) cell lines and clinical HCC samples.
RT-PCR and Western blot were used to detect the expressions of SUMO-1 in HCC cell lines, clinical HCC samples,and the non-neoplastic liver tissues adjacent to HCC. After transfection of SUMO-1 siRNA into HCC cell line SMMC-7721, the expression levels of Bcl-2, c-Myc and α-tubulin were examined, and MTT assay and cell cycle analysis were carried out as well.
Overexpressions of SUMO-1 were detected in HCC cell lines and clinical HCC samples, while the expression level of SUMO-1 in the non-neoplastic liver tissues was significantly lower (P < 0.001). Transfection of SUMO-1 siRNA resulted in 73.43% of maximal silencing efficiency of SUMO-1 in 48 h. The expressions of Bcl-2 and c-Myc were down-regulated coincidentally. SUMO-1 siRNA notably inhibited SMMC-7721 cells proliferation in vitro and increased the ratios of G2 phase and S phase in the cells.
Owing to overexpression of SUMO-1 in HCC and its important role in the development of HCC, SUMO-1 could be a latent target in diagnosis and therapy of HCC.
Journal of Cancer Research and Clinical Oncology 03/2011; 137(3):533-41. · 2.56 Impact Factor
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ABSTRACT: We investigated the role of XPD in cell apoptosis of hepatoma and its relationship with p53 during the regulation of hepatoma bio-behavior. RT-PCR and Western blot were used to detect the expression levels of XPD, p53, c-myc, and cdk2. The cell apoptosis and cell cycle were analyzed with flow cytometry. Compared with the control cells, XPD-transfected cells displayed a lower viability and higher apoptosis rate. A decreased expression of p53 gene was detected in XPD-transfected cells. In contrast, both c-myc and cdk2 showed increased expressions of mRNAs and proteins in the transfected cells. Our results indicate that XPD may play an important role in cell apoptosis of hepatoma by inducing an over-expression of p53, but suppressing expressions of c-myc and cdk2.
Medical Oncology 01/2011; 29(1):161-7. · 2.14 Impact Factor
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ABSTRACT: Although anoxic preconditioning (APC) in the myocardium has been investigated for many years, its physiological mechanism is still not completely understood. Increasing evidence indicates that transiently increased resistance to ischemic damage following APC is dependent on de novo proteins synthesis. However, the key effector pathway(s) associated with APC still remains unclear. The proto-oncogene Pim kinase belongs to a serine/threoine protein kinase family, consists of Pim-1, Pim-2 and Pim-3 and has been implicated in stimulating cell growth and inhibiting cell apoptosis. Therefore we assumed that Pim-3 expression might be aberrantly induced in cardiomyocytes that were subjected to anoxia/reoxygenation (A/R) injury and that Pim-3 might also contribute to cardio-protection after APC. To address this hypothesis, we cloned a Pim-3 expression vector, transfected it into rat cardiomyocytes, and examined Pim-3 expression in rat cardiomyocytes that were subjected to A/R injury. Moreover, we studied the role of three major MAPK pathways, e.g. p38 MAPK, JNK, and ERK1/2, in order to evaluate the molecular mechanism underlying Pim-3 up-regulation and A/R induced cardiomyocyte injury. Our experiments showed that APC induced an up-regulation of Pim-3 and the transfection of Pim-3 gene into the cardiomyocytes attenuated A/R injury. The inhibition of p38 MAPK by SB203580 abolished both the Pim-3 up-regulation and the cardio-protection provided by APC. Overall, these results suggest that APC could act to protect the heart from A/R injury with cooperation from the proto-oncogene Pim-3; in addition, it up-regulates Pim-3 expression through a p38 MAPK signaling pathway.
The international journal of biochemistry & cell biology 07/2009; 41(11):2315-22. · 4.89 Impact Factor
