CD44V6 regulates gastric carcinoma occurrence and development through up-regulating VEGF expression.

Abstract

Gastric carcinoma (GC) is one of the most common malignant tumors around the world. It is featured as high morbidity, poor prognosis, and short survival, thus seriously threats to the quality of life. The mechanism of GC is still unclear, leading to a difficulty in the treatment. CD44V6 plays an important role in tumorigenesis and progression, while its role in GC still needs further elucidation. GC tissue and para-carcinoma tissue were collected from patients in different tumor-mode-metastasis (TNM) stages. CD44V6 and vascular endothelial growth factor (VEGF) expressions were detected by real-time PCR and Western blot. Their correlations with the clinicopathological characteristics of GC were analyzed. GC cell line SGC-7901 was cultured in vitro and divided into control, scramble group, and CD44V6 small interfering RNA (siRNA) group. Cell proliferation was assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell apoptosis was evaluated by caspase 3 activity assay. CD44V6 and VEGF protein expressions significantly increased in GC tissue compared with adjacent normal control (p < 0.05). CD44V6 expression was correlated with differentiation, lymph node metastasis, and TNM staging (p < 0.05). CD44V6 was positively correlated with VEGF (p < 0.05). CD44V6 siRNA reduced CD44V6 and VEGF expressions in SGC-7901, inhibited cell proliferation, and enhanced caspase 3 activity compared with control (p < 0.05). CD44V6 participates in GC occurrence and development by up-regulating VEGF expression. Targeting CD44V6 regulates GC progression through inhibiting VEGF expression, promoting cell apoptosis, and restraining cell proliferation.