ABSTRACT
Objective:To investigate the effects of Porphyromonas gingivalis ( P. gingivalis) fimbrillin (FimA) on the progression of esophageal squamous cell carcinoma (ESCC). Methods:Wild-type P. gingivalis and fimA gene-deleted P. gingivalis ( fimA-/-P. gingivalis) were used to infect ESCC cells after morphology and PCR identification. Immunofluorescence, CCK-8 and Transwell chamber were used to detect the effects of FimA on the infectivity of P. gingivalis and it influences on cell invasion, proliferation and migration. Western blot was used to detect pSmad2/3 changes. The growth of tumor was detected in a nude mouse model bearing subcutaneous tumor. Results:Deletion of FimA might reduce the interbacterial adhesion of P. gingivalis. Compared with wild-type P. gingivalis, less fimA-/-P. gingivalis could infect NE6-T cells. Moreover, the proliferation, migration and invasion of NE6-T and KYSE30 cells as well as the activation of pSmad2/3 induced by P. gingivalis were inhibited after deletion of FimA. The growth of KYSE30 infected by fimA-/-P. gingivalis in nude mice was significantly slower than that of the wild-type P. gingivalis group. Conclusions:FimA mediated the effects of P. gingivalis on promoting the evolution of ESCC and was a potential target molecule to block the tumor-promoting effect of P. gingivalis.
ABSTRACT
@# Objective: To investigate the expression of long non-coding RNA NUP50-AS1 (lncRNA NUP50-AS1) in esophageal squamous cell carcinomas (ESCC) tissues and cell lines, and to explore its effect on proliferation, migration and invasion of human esophageal cancer Eca109 cells. Methods: 49 pairs of ESCC tissues and corresponding para-cancerous tissues obtained from the Biological Specimen Base of the Fourth Hospital of Hebei Medical University during Jan. 2015 to Jan. 2016 were used in this study. qRT-PCR method was applied to detect the expression of NUP50-AS1 in collected tissues samples and five esophageal cancer cell lines (TE1, TE13, Eca109, Kyse150 and Kyse170). ShRNAs were transiently transfected into Eca109 cells to interfere the expression of NUP50AS1 gene, and finally, sh2-NUP50-AS1 was used for the following experiments. The effect of NUP50-AS1 gene knockdown on the proliferation of Eca109 cells was detected by MTS and colony formation assay; the effect of NUP50-AS1 gene knockdown on the migration of Eca109 cells was detected by scratch test, and the effect on cell invasion was detected by Transwell assay. Results: The expression of NUP50-AS1 in ESCC was correlated with the lymphnode metastasis and TNM stage (all P<0.01). The expression of NUP50AS1 in ESCC tissues was significantly higher than that in corresponding normal tissues (2.003±0.870 vs 1.000±0.000, P<0.05). The expression of NUP50-AS1 in five esophageal cancer cell lines was significantly up-regulated (P<0.05), and it had the highest expression in Eca109 cell line. After transfection, sh2-NUP50-AS1 had the highest transfection efficiency, and knocking down NUP50-AS1 gene significantly inhibited the proliferation, invasion and migration of the Eca109 cells. Conclusion: The expression of lncRNA NUP50AS1 in ESCC tissues was significantly higher than that in the para-cancerous tissues, and correlated with the TNM stage and lymphnode metastasis. The down-regulation of NUP50-AS1 inhibited the proliferation, invasion and migration of esophageal cancer cells. The high expression of NUP50-AS1 gene may be closely related to the occurrence and development of ESCC.
ABSTRACT
Objective To investigate the relationship of the serum level of IL-23 and MMP-9 with the clinicopathologic features in patients with esophageal squamous cell carcinoma (ESCC). Methods 48 pathologically confirmed ESCC patients and 30 Endoscopic biopsy of benign were included in this study. The serum levels of IL-23 and MMP-9 were examined by enzyme-linked immunosorbent assay (ELISA). Results Serum IL-23 level in patients with ESCC was significantly higher than that in controls (t = 26.66, 16.89, P<0.05). Furthermore, Pearson′s correlation analysis revealed that serum IL-23 was positively correlated with the serum MMP-9 level in ESCC patients (r = 0.790, P < 0.05). Statistical analysis showed that enhanced serum IL-23 significantly correlated with the degree of differentiation and lymph node metastasis. Conclusion Overexpression of IL-23 may involve in the occurrence and development of ESCC. IL-23 may contribute to tumorinvasion and metastasis by stimulating the expression of MMP-9.