Differential expression of ANXA1 in benign human gastrointestinal tissues and cancers

被引:36
作者
Gao, Yunshu [1 ,2 ]
Chen, Ying [3 ]
Xu, Dongyun [1 ,4 ]
Wang, Jiejun [1 ]
Yu, Guanzhen [1 ]
机构
[1] Changzheng Hosp, Dept Med Oncol, Shanghai, Peoples R China
[2] 401 Hosp PLA, Dept Oncol, Qingdao, Shandong, Peoples R China
[3] Changhai Hosp, Dept Pathol, Shanghai, Peoples R China
[4] 97 Hosp PLA, Dept Oncol, Xuzhou, Jiangsu, Peoples R China
关键词
ANNEXIN A1 EXPRESSION; DECREASED EXPRESSION; DOWN-REGULATION; PROGRESSION; OVEREXPRESSION; ASSOCIATION; METASTASIS; ESOPHAGEAL; SURVIVAL; DISEASE;
D O I
10.1186/1471-2407-14-520
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
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页数:12
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