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MTSS1 inhibits metastatic potential and induces G2/M phase cell cycle arrest in gastric cancer.
Liu, Ke; Jiao, Xiao-Dong; Hao, Jie-Lu; Qin, Bao-Dong; Wu, Ying; Chen, Wei; Liu, Jun; He, Xi; Zang, Yuan-Sheng.
Afiliación
  • Liu K; Department of Medical Oncology, Changzheng Hospital, Naval Medical University, Shanghai, People's Republic of China.
  • Jiao XD; Department of Medical Oncology, Changzheng Hospital, Naval Medical University, Shanghai, People's Republic of China.
  • Hao JL; Department of Nephrology, Changzheng Hospital, Naval Medical University, Shanghai, People's Republic of China.
  • Qin BD; Department of Medical Oncology, Changzheng Hospital, Naval Medical University, Shanghai, People's Republic of China.
  • Wu Y; Department of Medical Oncology, Changzheng Hospital, Naval Medical University, Shanghai, People's Republic of China.
  • Chen W; Department of Pharmacy, Changzheng Hospital, Naval Medical University Shanghai, People's Republic of China.
  • Liu J; Department of Medical Oncology, Changzheng Hospital, Naval Medical University, Shanghai, People's Republic of China.
  • He X; Department of Medical Oncology, Changzheng Hospital, Naval Medical University, Shanghai, People's Republic of China.
  • Zang YS; Department of Medical Oncology, Changzheng Hospital, Naval Medical University, Shanghai, People's Republic of China.
Onco Targets Ther ; 12: 5143-5152, 2019.
Article en En | MEDLINE | ID: mdl-31303767
Background: Metastasis suppressor 1 (MTSS1), a potential metastasis suppressor gene associated with tumor progression, may play an important role in cancer development. Our previous study demonstrated that MTSS1 was downregulated significantly when gastric cancer (GC) progressed and metastasized, suggesting that MTSS1 may be involved in the physiopathologic mechanism of GC. Purpose: The objective of this study was to evaluate the effect of MTSS1 expression on the biological behavior of gastric cancer cell both in vitro and in vivo. Materials and methods: The gain-and-loss function of MTSS1 in GC cells were analyzed after transfection with pEGFP-N1-MTSS1 and ShRNA431. Proliferation and invasion abilities were measured by means of plate clone formation assay and transwell assay. To further explore the underlying mechanism of MTSS1-induced tumor restrain, cell cycle distribution was analyzed using flow cytometry. Results: The results revealed that overexpression of MTSS1 significantly reduced proliferation, migration and invasion of GC cells in vivo and in vitro, while downregulation of MTSS1 had the opposite biological manifestations. Moreover, overexpression of MTSS1 induced accumulation of GC cells in G2/M phase, increased phosphorylated Cdc2 expression and decreased Cdc25C and cyclinB1 levels, suggesting MTSS1 could cause G2/M cell cycle arrest. Conclusion: Our data provided insight into an important role for MTSS1 in suppressing tumor cell proliferation, invasion and migration, indicating that MTSS, as a functional tumor suppressor in GC, could be a potential therapeutic target to prevent GC metastasis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Onco Targets Ther Año: 2019 Tipo del documento: Article Pais de publicación: Nueva Zelanda
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Onco Targets Ther Año: 2019 Tipo del documento: Article Pais de publicación: Nueva Zelanda