Downregulation of programmed cell death 4 (PDCD4) in tumorigenesis and progression of human digestive tract cancers

被引:35
作者
Ma, Gang [1 ]
Zhang, Hao [1 ]
Dong, Ming [1 ]
Zheng, Xinyu [1 ]
Ozaki, Iwata [2 ]
Matsuhashi, Sachiko [3 ]
Guo, Kejian [1 ]
机构
[1] China Med Univ, Affiliated Hosp 1, Dept Surg, Shenyang, Peoples R China
[2] Saga Univ, Saga Med Sch, Dept Internal Med, Div Hepatol & Metab, Saga 840, Japan
[3] Saga Univ, Saga Med Sch, Hlth Adm Ctr, Saga 840, Japan
基金
中国国家自然科学基金;
关键词
PDCD4; Digestive tract cancers; Western blot; RT-PCR; Immunohistochemistry; HUMAN HEPATOCELLULAR-CARCINOMA; SUPPRESSOR PDCD4; BREAST-CANCER; TRANSFORMATION SUPPRESSOR; TRANSLATION INITIATION; AP-1; TRANSACTIVATION; INHIBITS TRANSLATION; ESOPHAGEAL CANCER; GENE-EXPRESSION; PROTEIN;
D O I
10.1007/s13277-013-0975-9
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Nowadays, digestive tract cancers become the commonest neoplasia and one of the leading causes of cancer deaths worldwide. The development of diagnosis and therapy is urgently required. Programmed cell death 4 (PDCD4), a new tumor suppressor, has been documented to be a potential diagnostic tool and treatment target for neoplasia due to the inhabitation of tumor promotion/progression and metastasis. However, its role in human digestive tract cancers is few available up to now. In this study, we examined the expression of PDCD4 in human digestive tract cancers (61 gastric cancer, 65 colorectal cancer, and 69 pancreatic cancer patients) by Western blot analysis, reverse transcription (RT)-PCR, and immunohistochemistry. Western blot, RT-PCR, and immunohistochemistry examination showed that expressions of PDCD4 were significantly lower in cancers specimens than in noncancerous tissues. Among the different differentiated cancer tissues, PDCD4 expression was significantly lower in moderately or poorly differentiated cancers than in well-differentiated cancers (p < 0.05). Our findings suggested that PDCD4 might be a potentially valuable molecular target in diagnosis and therapy for human digestive tract cancers.
引用
收藏
页码:3879 / 3885
页数:7
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