Open Access Research article

Differential expression of ANXA1 in benign human gastrointestinal tissues and cancers

Yunshu Gao12, Ying Chen3, Dongyun Xu14, Jiejun Wang1* and Guanzhen Yu1*

Author Affiliations

1 Department of Medical Oncology, Changzheng Hospital, Shanghai, China

2 Department of Oncology, 401 Hospital of PLA, Qingdao, Shandong Province, China

3 Department of Pathology, Changhai Hospital, Shanghai, China

4 Department of Oncology, the 97 Hospital of PLA, Xuzhou, Jiangsu Province, China

For all author emails, please log on.

BMC Cancer 2014, 14:520  doi:10.1186/1471-2407-14-520

Published: 19 July 2014

Abstract

Background

Annexin-1 contributes to the pathological consequence and sequelae of most serious human diseases including cardiovascular disease and cancer. Although diverse roles in carcinogenesis have been postulated, its role in human gastrointestinal cancers still remains controversial.

Methods

The mRNA and protein expression profiles of ANXA1 were studied in human esophageal, gastric, pancreatic, colorectal, liver, and bile duct cancers using Real-Time PCR, western blotting, and immunohistochemistry. Gain/loss-of-function by pcDNA3.1-ANXA1 and ANXA1-shRNA was performed in gastric cancer cells.

Results

ANXA1 was widely expressed in adult gastrointestinal tissue. All methods showed that ANXA1 was down-regulated in esophageal, gastric, and bile duct cancers, but up-regulated in pancreatic cancer. Forced ANXA1 expression in gastric cancer cells leads to cell growth inhibition and concomitantly modulates COX-2 expression. We confirm loss of ANXA1 and overexpression of COX-2 in clinical gastric cancer, suggesting that the anti-proliferative function of ANXA1 against COX-2 production might be lost.

Conclusions

ANXA1 expression is “tumor-specific” and might play a multifaceted role in cancer development and progression. ANXA1 was widely expressed in normal gastrointestinal epithelium, suggesting its role in the maintenance of cellular boundaries. Furthermore, ANXA1 regulates GC cell viability via the COX-2 pathway.