Expression of FMNL2 and its relation to the metastatic potential of human colorectal cancer cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the association of FMNL2 expression with the metastatic potential of colorectal cancer cells.</p><p><b>METHODS</b>FMNL2 mRNA and protein expressions in 6 human colorectal cancer cell lines were detected by real-time RT-PCR and immunohistochemical method, respectively, and analyzed for their correlations to the in vitro invasiveness of the cell lines evaluated by Boyden assay. In SW620 and SW480/M5 cell lines, the expression of FMNL2 was repressed by FMNL2 short hairpin RNA (shRNA), and the changes in the invasiveness of the cells were observed.</p><p><b>RESULTS</b>FMNL2 was highly expressed in SW480/M5, LoVo and SW620 cells derived from metastatic colorectal cancers in comparison with that in LS174T, SW480 and HT29 cells, which were derived from primary colorectal cancers. In vitro analysis of the cell invasiveness demonstrated that SW480/M5, LoVo and SW620 cells had higher invasiveness than LS174T, SW480 and HT29 in vitro. In SW480/M5 and SW620 cells, transfection with FMNL2 shRNA resulted in significantly lowered cell invasiveness.</p><p><b>CONCLUSION</b>FMNL2 may play an important role in the invasion and metastasis of colorectal cancer.</p>

Galectin-1 expression in human colorectal carcinoma and its clinical significance / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the correlation between galectin-1 expression and the biological behaviors of human colorectal carcinoma.</p><p><b>METHODS</b>SP immunohistochemistry was used to detect the expression of galectin-1 in 158 paraffin-embedded specimens including 30 normal mucosa, 25 adenoma, 65 colorectal carcinoma and 38 metastatic tumor specimens. Real-time RT-PCR was used to detect galectin-1 mRNA expression in 32 fresh specimens of colorectal carcinoma and normal mucosa.</p><p><b>RESULTS</b>The positive expression level of galectin-1 was significantly different between normal mucosa, adenoma, colorectal carcinomas and metastatic tumors, with positivity rate of 0, 8%, 66% and 86%, respectively (P<0.05). Galectin-1 expression in moderately or well differentiated colorectal carcinomas was significantly lower than that in poorly differentiated ones (P=0.031), and its expression in invasive carcinomas was significantly higher than that in non-invasive carcinomas (P=0.000). Galectin-1 expression in colorectal carcinomas was significantly related with lymph node metastasis (P=0.004). In poorly differentiated colorectal carcinomas, the expression of galectin-1 mRNA was about 2.27 times that in moderately or well differentiated colorectal carcinomas (P=0.00); galectin-1 mRNA expression in invasive carcinoma was 1.98 times that in non-invasive carcinoma (P=0.002). In tumors with lymph node metastasis, galectin-1 mRNA expression was 1.42 times that in tumors without metastasis (P=0.018).</p><p><b>CONCLUSION</b>Galectin-1 can be involved in the development and progression of colorectal carcinoma, and may relate to the infiltration, differentiation and lymph node metastasis of colorectal carcinoma.</p>

Effect of AcSDKP on the proliferation and collagen synthesis in cultured rat cardiac fibroblasts stimulated by PDGF / 中国应用生理学杂志

<p><b>AIM</b>To investigate whether AcSDKP can inhibit proliferation and collagen synthesis in cultured rat cardiac fibroblasts mediated by PDGF.</p><p><b>METHODS</b>Neonatal rat cardiac fibroblasts were isolated. The cell proliferation was observed by 3H-proline incorporation assay.</p><p><b>RESULTS</b>On the culture of 0.4% FBS, PDGF stimulated cardiac fibroblasts proliferation and collagen synthesis with a dose-dependent manner at the concentrations from 1 ng/ml to 20 ng/ml, in which 10 ng/ml PDGF reached its peak. AcSDKP at the concentration from 10(-10) mol/L to 10(-8) mol/L could inhibit cardiac fibroblasts proliferation and collagen synthesis mediated by PDGF. 10(-9) mol/L AcSDKP attained its peak on inhibiting cardiac fibroblasts proliferation and collagen synthesis.</p><p><b>CONCLUSION</b>AcSDKP can inhibit proliferation and collagen synthesis in cultured rat cardiac fibroblasts mediated by PDGF.</p>

Role of AcSDKP on collagen synthesis and degradation in cultured rat cardiac fibroblast / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the role of AcSDKP on collagen synthesis and degradation in cultured rat cardiac fibroblasts.</p><p><b>METHODS</b>Neonatal rat cardiac fibroblasts were isolated and stimulated by PDGF. The cell proliferation was observed by (3)H-TdR incorporation assay. The synthesis of collagen was measured by (3)H-proline incorporation assay. The expression of type I and type III collagen and MMP-1 protein were measured by Western blot. The MMP-2 and MMP-9 activity was evaluated with zymography assay.</p><p><b>RESULTS</b>PDGF stimulated cardiac fibroblasts proliferation with increased collagen synthesis and type I and type III collagen protein expressions as well as MMP-2 and MMP-9 activities and MMP-1 expression. AcSDKP inhibited cardiac fibroblasts proliferation induced by PDGF and reduced collagen synthesis and type I and type III collagen protein expression. AcSDKP also further up-regulated MMP-2 and MMP-9 activities and MMP-1 expression in cardiac fibroblasts induced by PDGF.</p><p><b>CONCLUSION</b>AcSDKP inhibited proliferation and collagen synthesis and up-regulated matrix metalloproteinases activity or expression induced by PDGF, which was possibly related with the effect of AcSDKP anti-fibrosis.</p>