Expression analysis and clinical significance of eIF4E, VEGF-C, E-cadherin and MMP-2 in colorectal adenocarcinoma
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Minna Gao1,*, Xiong Zhang2,*, Dan Li3, Ping He4, Wenguang Tian4, Bo Zeng5
1Department of Pathology, Chongqing Medical University, Chongqing 400016, China
2College of Basic Medicine, Chongqing Medical University, Chongqing 400016, China
3Department of Critical Care Medicine, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China
4Department of Infectious diseases, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China
5Department of Gastroenterology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China
*These authors have contributed equally to this work
Bo Zeng, email: [email protected]
Keywords: colorectal cancer, eIF4E, VEGF-C, MMP-2, E-cadherin
Received: June 29, 2016 Accepted: October 27, 2016 Published: November 19, 2016
The underlying mechanisms of colorectal carcinoma (CRC) metastasis remain to be elucidated. The aim of this study is to investigate clinical significance and the expression of eIF4E, VEGF-C, MMP-2, and E-cadherin in the CRC metastasis. We investigated their expressions in 108 patients, analyzed the relationships between their expressions in CRC and evaluated the relationships between their expressions and clinical pathogenic parameters. Furthermore, their roles in patient survival and in CRC metastasis were also investigated. We found that eIF4E, VEGF-C and MMP-2 were up-regulated in CRC, and their expression frequencies (EFs) were higher in cancerous tissues than in adjacent normal tissues. The EF of E-cadherin is lower in cancerous tissues than in adjacent normal tissues. Totally, their EFs were not associated with sex and age of patient, however, their EFs were associated with tumor differentiation, the depth of invasion, lymph node metastasis and tumor stages. Furthermore, eIF4E, VEGF-C, and MMP-2 shortened and E-cadherin prolonged survival in patient-derived CRC xenografts. Similarly, eIF4E, VEGF-C, and MMP-2 promoted and E-cadherin suppressed the lung metastasis of CRC cells. In addition, knockdown of eIF4E inhibited migration of CRC cells, downregulated VEGF-C, MMP-2 and upregulated E-cadherin. In conclusion, eIF4E promoted CRC metastasis via up-regulating the expression of VEGF-C, MMP-2 and suppressing E-cadherin.
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