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Gu Y.-P.,Soochow University of China | Zhao Y.-G.,Second Peoples Hospital of Changshu | Zhu Y.-B.,Soochow University of China | Zhang G.-B.,Soochow University of China | Huang J.-A.,Soochow University of China
Chinese Journal of Cancer Prevention and Treatment

OBJECTIVE: To investigate the expression of TROP-2 in human pulmonary adenocarcinoma (ADC) tissues and cell lines. METHODS: TROP-2 expression was detected by flow cytometry in five ADC cell lines and one immortalized human bronchial epithelial cell line HBE. TROP-2 mRNA was examined in 11 patients with ADC and also analyzed immunohistochemically in 46 patients with ADC. Furthermore, the correlations between TROP-2 and clinicopathologic features and prognosis of ADC were analyzed. RESULTS: TROP-2 was detected in H1975, SPCA-1 and PC-9, but not in A549, H1299 and HBE. The expression of TROP-2 in H1975, SPCA-1, PC-9 respectively were (45.3±5.4)%, (91.4±4.6)% and (97.2±2.1)%. TROP-2 mRNA expression in ADC tissues detected by RT-PCR was 72.7%(8/11). TROP-2 expression detected immunohistochemically was significantly increased in ADC tissues (43.5%, 20/46) than that in tumor- adjacent normal tissues (0) and in benign lesions (9.5%, 2/21; P=0.001). The overexpression of TROP-2 was correlated with lymph node metastasis (P=0.02) and TNM stage (P=0.02). TROP-2 tended to be expressed in cases with an unfavorable outcome (P=0.068). CONCLUSION: TROP-2, which is highly expressed in pulmonary ADC tissues and cell lines, may be involved in carcinogenesis. Source

Zheng J.,Second Peoples Hospital of Changshu | Guo Z.,Second Peoples Hospital of Changshu | Li L.,Second Peoples Hospital of Changshu | Song M.,Second Peoples Hospital of Changshu | And 2 more authors.
Chinese Journal of Clinical Oncology

Objective: To investigate the influence of platelet-derived growth factor D (PDGFD) on the proliferation of BEL-7402 human liver tumor cells and the expression of vascular endothelial growth factor (VEGF). Methods: Human liver tumor cell strain BEL-7402 and paracarcinoma cell strain QSG-7701 were cultured in vitro. PDGF-D and PDGFRβ mRNA expression were assessed by reverse transcription-polymerase chain reaction (RT-PCR). BEL-7402 was treated with different concentrations (0, 5, 10, 20, 50, 100, and 200 μg/mL) of exogenous PDGF-D. Cell proliferation was measured using the MTT assay. The effect of exogenous PDGF-D on the cell cycle of BEL-7402 cells was assessed by flow cytometry. The expression of VEGF was detected by RT-PCR and ELISA in BEL-7402 cells that were exposed to different concentrations of PDGF-D. Results: PDGF-D and PDGFRβ mRNA expression in human liver tumor cell strain BEL-7402 was considered significantly higher than that in paracarcinoma cell strain QSG-7701 (P<0.05). Exogenous PDGF-D promoted proliferation of tumor cells in a dose-dependent manner from 10 μg/mL to 100 μg/mL (P<0.05). The effect of PDGF-D at 100 μg/mL was stronger than at other concentrations. Incubation of tumor cells with PDGF-D markedly decreased the percentage of cells in G 0/G1-phase and increased the percentage of cells in S-phase. Compared with the control group, VEGF and PDGFRβ mRNA expression in the experimental groups (PDGF-D from 10 μg/mL to 200 μg/mL) was increased (P<0.05). VEGF protein expression in the experimental groups was significantly enhanced by exogenous PDGF-D in a dose-dependent manner, except in the 5 μg/mL group. Similarly, VEGF protein expression in the experimental groups was significantly higher than that in the control group. Conclusion: PDGF-D can promote proliferation of hepatocarcinoma BEL-7402 cells and increase expression of VEGF in a dose-dependent manner. PDGF-D may play an important role in the development of HCC and can be used as an index for prognosis evaluation and a target of treatment for liver cancer. Source

Huang J.,Second Peoples Hospital of Changshu | Yang J.,Soochow University of China | Ling C.,Soochow University of China | Zhao D.,Soochow University of China | And 2 more authors.
Chinese Journal of Lung Cancer

Background and objective The inhibitor of growth 4 (ING4) is an important tumor suppressive gene. It has been proven that ING4 could inhibite the proliferation of many tumors. The aim of this study is to investigate the inhibitory effect and anti-cancer mechanism of adenovirus-mediated ING4 gene on SPC-A1 human lung adenocarcinoma in nude mice. Methods A human lung adenocarcinoma xenograft model was established with SPC-A1 cells in nude mice. A total of 15 tumor-bearing nude mice were randomly divided into three groups, namely, PBS, Ad-GFP, and Ad-ING4. The mice in the three groups were intratumorally injected every other day. Their tumor volumes were continually recorded. The treatment tumors were then removed from the mice and weighed. Tumor inhibition rates were calculated. Cell apoptosis was examined by TUNEL method. Caspase-3, COX-2, Fas, and FasL expressions were investigated by immunohistochemistry SP assay. Results Both tumor weight and volume in the Ad-ING4 group were significantly decreased. The tumor inhibition rate of the mice in the Ad-ING4 group (33.17%±5.24%) was statistically different from that of the mice in the Ad-GFP group (1.31%±0.31%; P<0.05). The apoptotic index of the mice in the Ad-ING4 group (69.23%±6.53%) was also significantly different from those in PBS (17.04%±1.10%) and Ad-GFP groups (18.81%±1.93%; P<0.05). Based on immunohistochemistry SP assay, the results showed that Ad-ING4 may not only upregulate the expressions of caspase-3, Fas, and FasL but also downregulate the expression of COX-2. Conclusion ING4 gene elicited a remarkable growth inhibitory effect on human lung adenocarcinoma xeno-gras in nude mice. e mechanism is possibly related to an increase in tumor cell apoptosis. Source

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