Expression of miR-143 in nasopharyngeal carcinoma cell lines and its effect on cell adhesion ability / 南方医科大学学报

<p><b>OBJECTIVE</b>To detect miR-143 expression in human nasopharyngeal carcinoma (NPC) cell lines and explore the role of miR-143 in regulating the adhesion ability of NPC cells.</p><p><b>METHODS</b>Fluorescence quantitative RT-PCR was used to detect miR-143 expression levels in 5 NPC cell lines (CEN1, CNE2, HONE1, 5-8F, and 6-10B) and an immortalized human nasopharyngeal epithelial cell line (NP69). The retrovirus plasmid pMSCV-puro-miR-143 was constructed and the packaged retroviruses pMSCV-puro and pMSCV-puro-miR-143 were infected in 5-8F cells to establish a cell line with stable miR-143 overexpression, whose adhesion ability was tested with adhesion assay.</p><p><b>RESULTS</b>The expression of miR-143 was down- regulated in the NPC cell lines, and the highly metastatic NPC cell line 5-8F had a expression of only 3.0% of the control level, as compared with the level of 63.59% in the tumorigenic but nonmetastatic NPC cell line 6-10B. The transfected 5-8F cells showed a 1080-fold increase of miR-143 expression (P<0.05) with a significantly lowered adhesion ability.</p><p><b>CONCLUSION</b>miR-143 plays a role in regulating the invasiveness and metastasis of NPC, and overexpression of miR-143 causes a significant reduction of the adhesion ability of the highly metastatic NPC cell line 5-8F.</p>

MiR-143 inhibits migration of human nasopharyngeal carcinoma cells by negatively regulating GLI3 gene / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the possible biological function and mechanism of miR-143 in the metastasis of human nasopharyngeal carcinoma (NPC).</p><p><b>METHODS</b>Using bioinformatics to predict the target gene of miR-143, the 3'UTR and mutant 3'UTR of GLI3 gene was cloned into psiCHECK-2 vector. Dual-luciferase reporter gene assay was employed to examine the repression of the GLI3 gene. miR-143 and GLI3 expression levels in 5-8F cells transfected with miR-143 mimics, inhibitor, or siGLI3 were examined, and the changes in the cell migration ability was assessed by Transwell invasion assay.</p><p><b>RESULTS</b>Bioinformatics prediction indicated the Hh pathway transcription gene GLI3 as a target gene of miR-143, and dual-luciferase reporter assay showed that miR-143 directly combined with the 3'UTR of GLI3. qRT-PCR and Western blotting demonstrated that the expression of miR-143 in 5-8F cells was negatively correlated to GLI3 and suppressed the migration of 5-8F cells.</p><p><b>CONCLUSION</b>MiR-143 can inhibit the invasion of NPC cells by negative regulation of GLI3 gene, which sheds light on the role of miR-143 and Hh pathway in NPC.</p>

Role of centromere protein H in human gastric cancer cell proliferation / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the role of centromere protein H (CENP-H) in the proliferation of human gastric cancer cells.</p><p><b>METHODS</b>RT-PCR and Western blot analysis were employed to examine the mRNA and protein expressions of CENP-H in 7 human gastric cancer cell lines and immortalized human gastric epithelial cells (GES-1). The cells were infected with the retrovirus vectors pMSCV-CENP-H or CENP-H-RNAi to establish stable cell lines with high CENP-H expression or CENP-H expression interference. MTT assay and colony formation assay were used to examine the changes in the cell proliferation after the infection.</p><p><b>RESULTS</b>CENP-H was over-expressed in gastric cancer cell lines AGS, BGC823, SGC-7901, MKN45, HGC27, MGC-803 and MKN28 at both mRNA and protein levels. The established AGS/CENP-H cell line with increased CENP-H expression showed enhanced proliferative activity, while the cell line MGC-803/CENP-H-RNAi with CENP-H expression interference showed an obviously lowered proliferation ability.</p><p><b>CONCLUSION</b>CENP-H promotes the proliferation of human gastric cancer cells, suggesting its important role in the occurrence and development of gastric cancer.</p>

Therapeutic effect of axitinib and 5-FU in nude mice bearing human colon cancer xenograft / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the inhibitory effect and toxicity of axitinib combined with 5-FU in nude mice bearing transplanted tumor of colon cancer LoVo cells.</p><p><b>METHODS</b>Nude mouse models bearing LoVo colon cancer xenograft were randomized into vehicle control group, untreated control group, axitinib-treated group, 5-FU-treated group and combined treatment group for corresponding treatments. The tumor dimensions, body weight and tumor weight were recorded, and the efficacy and toxicity were evaluated in terms of complete remission (CR), partial remission (PR), tumor growth delay (TGD), mortality rate and net body weight loss.</p><p><b>RESULTS</b>The combined treatment showed a significantly stronger efficacy than axitinib or 5-FU used alone. TGD of the combined treatment group was 16.73 days, longer than that of axitinib (8.53 days) and 5-FU (9.72 days) used alone. No mouse died during the treatments in the untreated control group, and 1 died in each of the other 4 groups. The mortality rate and weight loss were both less than 20%. One mouse had PR in axitinib-treated group and another in the combination treatment group. Axitinib, alone and in combination with 5-FU, reduced ABCG2 expression in the tumor tissue, and 5-FU has no such effect.</p><p><b>CONCLUSION</b>Combination of axitinib and 5-FU produces better antitumor effect than either drug used alone and is well tolerated in nude mice bearing colon cancer xenograft.</p>

EVALUATION OF CLINICAL VALUE OF TISSUE POLYPEPTIDE SPECIFIC ANTIGEN (TPS)ASSAY IN GASTRO-INTESTINAL CARCINOMAS / 解放军医学杂志

To investigate the expression and clinical value of serum TPS(tissue polypeptide specific antigen) assay in patients with gastrointestinal tract tumor. Fifty six patients with gastrointestinal tract tumors were studied in contrast with 114 healthy people. The levels of serum TPS, CEA, and CA199 were assayed with ELISA. The results showed that the levels and positive rates of serum TPS, CEA and CA199 were significantly higher in gastrointestinal tract tumor group than those in the normal healthy group ( P