Prognosis of gastric adenocarcinoma associated with girdin, Akt, and cortactin.

Abstract

Background: The actin-binding protein girdin regulates tumor cell migration and invasion by maintaining actin structure. PI3K/Akt signaling is an important actin-remodeling pathway. The protein cortactin acts directly on microfilaments and promotes tumor invasion and metastasis by rearranging the cytoskeleton. However, there are few reports on the co-expression of girdin, Akt, and cortactin in gastric adenocarcinoma (GAC).

Objectives: Evaluate girdin, Akt, and cortactin expression in GAC tissues and assess their relationship to the prognosis of GAC patients.

Design: Survival analysis SETTING: Medical college in China PATIENTS AND METHODS: We compared survival in 110 paraffin-preserved GAC with corresponding normal gastric mucosa tissues in relationship to girdin, Akt, and cortactin expression levels.

Main outcome measure: Expression levels of the proteins.

Sample size: 110 RESULTS: The expression of girdin, Akt, and cortactin were all upregulated in GAC tissues compared with corresponding normal tissues (66.4% vs 36.3%, 57.3% vs 28.2% and 69.1% vs 22.7%, respectively; P<.05) and expression was mutually positive (all P<.05). Overall survival in the girdin, Akt, and cortactin high expression groups was reduced. Multivariate analysis showed that girdin, Akt, cortactin, lymph node metastasis (LNM) and TNM stages were independent factors affecting GAC patients prognosis (P<.05).

Conclusions: Girdin and cortactin may promote GAC invasion and metastasis via the PI3-K/Akt signaling pathway. Girdin, Akt, and cortactin co-expression might serve as a novel molecular target for GAC therapy and improve the prognosis of patients with this disease.

Limitations: A small sample size and lack of related research on molecular mechanisms.

Conflict of interest: None.