Wei-Jia Sun

Central South University, Changsha, Hunan, China

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Publications (3)3.46 Total impact

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    ABSTRACT: Abstract Background: Pancreatic cancer has poor prognosis and high mortality. Currently, the therapy of pancreatic cancer remains a challenge. In this study, we compared the antitumor activity of the recombinant antitumor antiviral protein (RAAP), an improved interferon, with gemcitabine, a classic chemotherapy agent used for pancreatic cancer treatment. Methods: The proliferation of Bx-PC3 pancreatic cancer cells was evaluated by an MTT assay. Cell cycle arrest and apoptosis were evaluated by flow cytometry and annexin V-FITC/propidium iodide double staining, respectively. The expressions of matrix metalloproteinase (MMP)-2, MMP-9, caspase-3, caspase-8, and caspase-9 genes were evaluated by reverse transcription-polymerase chain reaction and the Western blot analysis. A xenograft pancreatic cancer model was established by inoculating Bx-PC3 cells into athymic nude mice. The antitumor activity of RAAP and gemcitabine was tested in the xenograft tumor model. Results: RAAP significantly inhibited proliferation, induced cell cycle arrest, and induced apoptosis in Bx-PC3 cells in vitro and delayed tumor growth in vivo. The antitumor activity of 20 ng/mL of RAAP was a little more effective than 10 μM of gemcitabine. The antitumor activity of RAAP was associated with its role in inducing caspase-3 and caspase-8 expression as well as downregulating MMP-2 expression. Conclusions: RAAP can effectively suppress human pancreatic cancer cell growth in vitro and in vivo. The antitumor efficacy of RAAP is similar to gemcitabine.
    Cancer Biotherapy & Radiopharmaceuticals 07/2012; 27(7):426-33. · 1.44 Impact Factor
  • Kun Song, Bin Li, Wei-jia Sun
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    ABSTRACT: To compare the efficacy of gemcitabine (GEM) alone and gemcitabine based combination chemotherapy (GEMCOM) on advanced pancreatic cancer. Keywords Phase III, gemcitabine and pancreatic cancer were used to search and collect Phase III-randomized references about gemcitabine and gemcitabine-based combination chemotherapy applied on advanced pancreatic cancer. A references-based meta-analysis was made to compare the efficacy between GEM and GEMCOM. Before that, test for heterogeneity was committed. Fixed effect model was used if the I(2) ≤ 50%, and random effect model was used if not. The evaluating indicators were overall response rate and 1-year survival rate. There were 14 randomized controlled trial (RCT) and 10 RCT enrolled in overall response rate analysis and 1-year survival rate analysis, respectively. Results of meta-analysis showed that, arm GEMCOM's overall response rate and 1-year survival rate were higher than arm GEM's (z = 2.190, P = 0.028 vs. z = 4.400, P = 0.000). The differences were significant. The biases of the results were tested by Egger-test. The tests showed that no bias exists in both of two meta-analysis (t = 0.070, P = 0.946 and t = -0.740, P = 0.483) respectively. There is a possibility that the gemcitabine-combination is more effective than the gemcitabine on overall response rate and 1-year survival rate.
    Zhonghua wai ke za zhi [Chinese journal of surgery] 09/2011; 49(9):839-42.
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    ABSTRACT: The present experiments sought to determine whether cilostazol, a selective inhibitor of cyclic adenosine monophosphate (cAMP) phosphodiesterase 3 (PDE3), suppressed elastase-induced abdominal aortic aneurysm (AAA) development in a rat model. Male Sprague-Dawley rats (n = 16/each group) were randomly distributed into three groups: sham-, saline-, and cilostazol-. Rats of saline and cilostazol groups underwent intra-aortic elastase perfusion to induce AAAs, while rats of sham-group were perfused with saline. Rats of cilostazol-group received cilostazol treatment (100 mgkg(-1)d(-1)) for the entire experimental period. The areas of the lumen of the aortas at the segment with maximum diameter were measured preperfusion and on d 7, 14 after perfusion. Systolic blood pressure was measured by tail-cuff technique. Aortic tissue samples were harvested on d 14 after intra-aortic perfusion and evaluated by reverse transcription-polymerase chain reaction and Western blot for matrix metalloproteinase-2, 9 (MMP-2, 9), by immunohistochemistry for nuclear factor kappa B (NF-κB), and by Gomori aldehyde fuchsin for elastin. Activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and level of reactive oxygen species (ROS) in these samples were also measured. On d 14, rats of saline-group had significantly increased aortic sizes compared with sham-group (P < 0.01), while, cilostazol treatment significantly reduced this increase (cilostazol- versus saline-, P < 0.01) without affecting blood pressure (P > 0.05). The expression of both MMP-2 and MMP-9 and the destruction of elastic fibers in aortic tissues were significantly decreased by cilostazol treatment (P < 0.05), probably through the suppression of NF-κB activation (P < 0.01). Consistently, cilostazol significantly inhibited NADPH oxidase activity (P < 0.01), accompanied by a reduced level of ROS (P < 0.01). Cilostazol retards experimental AAAs development independently of blood pressure reduction possibly by inhibiting proteolysis, inflammation, and oxidative stress. Selective PDE3 inhibition may offer an additional method to pharmacologically inhibit AAAs.
    Journal of Surgical Research 02/2011; 167(2):e385-93. · 2.02 Impact Factor