Myeloid ecotropic viral integration site 1 inhibits cell proliferation, invasion or migration in human gastric cancer
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Fei Song1, Hong Wang1 and Yingying Wang2
1Department of General Surgery, Shandong Provincial Third Hospital, Jinan, Shandong, China
2Department of Gynecologic Oncology, Shandong Cancer Hospital Affiliated to Shandong University, Shandong Academy of Medical Sciences, Jinan, Shandong, China
Yingying Wang, email: firstname.lastname@example.org
Keywords: MEIS1, gastric cancer, proliferation, invasion, migration
Received: June 27, 2017 Accepted: September 05, 2017 Published: September 28, 2017
Myeloid ecotropic viral integration site 1 (MEIS1) has been identified to be a potential tumor suppressor in some cancers. However, the mechanisms underlying MEIS1-induced cancer development and progression were not clear. Here, we investigated the expression and role of MEIS1 in gastric cancer. In vivo, we analyzed tumor growth using nude mice model. In the present study, MEIS1 expression was obviously decreased in GC cell lines compared with that in normal gastric cell lines (all p<0.001). MEIS1 overexpression inhibited cell proliferation and G1/S transition accompanied by decreased Cyclin D1 and Cyclin A expression. Furthermore, MEIS1 overexpression decreased the expression of Survivin, and induced cell apoptosis (p<0.001). Transwell migration assay revealed that MEIS1 affects cell invasion and migration, and inhibited epithelial-mesenchymal transition (EMT). Finally, MEIS1 inhibits MKN28 cell growth in nude mice model. In conclusion, our study suggested that MEIS1 plays an important role in regulating cell survival, proliferation, anchorage-independent growth, cell cycle, apoptosis and metastasis. Thus, MEIS1 might be recommended as an effective target for GC patients.
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