Aim: To investigate the expression of Ras homolog (Rho)C, vascular endothelial growth factor (VEGF) and CD105 in esophageal squamous cell carcinoma.
Methods: Semi-quantitative reverse transcriptase polymerase chain reaction, in situ hybridization and immunohistochemical streptavidin-biotin- peroxidase methods were used to detect expression of RhoC mRNA and protein, and VEGF protein in 62 cases with esophageal squamous cell carcinoma, 31 cases with adjacent atypical hyperplastic tissues, and 62 cases with normal esophageal mucosa. CD105 antibody labeling was used to measure microvascular density. Expression levels were compared according to clinicopathologic and patient parameters.
Results: Expression of RhoC mRNA showed a positive correlation with the protein level in esophageal squamous cell carcinoma, as well as with VEGF protein levels. RhoC mRNA expression was mainly located within the cytoplasm of the tumor cells, appearing as blue to purple particles by in situ hybridization. The differences in RhoC mRNA expression in esophageal squamous cell carcinoma, adjacent atypical hyperplasia and normal esophageal mucosa were significant (P < 0.05). The relative expression of RhoC mRNA in cancer tissues with lymph node metastasis was significantly higher than in the tissues without lymph node metastasis (P < 0.05). VEGF protein expression was consistent with microvascular density (t = 25.52, P < 0.05). Positive expression of VEGF protein in esophageal squamous cell carcinoma of different histologic gradings did not differ significantly. Positive expression of VEGF protein in carcinoma tissues with deep infiltration was significantly higher than in tissues with only superficial infiltration (P < 0.05). The positive expression of VEGF protein in cancer tissues with lymph node metastasis was significantly higher than in the tissues without lymph node metastasis (P < 0.05).
Conclusion: RhoC protein may upregulate VEGF expression, thereby promoting tumor angiogenesis. RhoC mRNA and protein expression was correlated with metastasis.
Keywords: Esophageal squamous cell carcinoma; Gene silencing; Ras homolog C; Vascular endothelial growth factor.