CMTM3 is reduced in prostate cancer and inhibits migration, invasion and growth of LNCaP cells
Clin. transl. oncol. (Print)
; Clin. transl. oncol. (Print);17(8): 632-639, ago. 2015. tab, ilus
Article
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| IBECS
| ID: ibc-138178
Biblioteca responsable:
ES1.1
Ubicación: BNCS
ABSTRACT
Purpose. A novel tumor suppressor gene CKLF-like MARVEL transmembrane domain-containing member 3 (CMTM3) is reduced or undetectable in many kinds of cancers and relates tumor malignant features. We detected its role in prostate cancer for possibility of target therapy as accumulating evidence has shown that CMTM3 is a promising tumor suppressor gene (TSG) for gene therapy. Methods. The expression of CMTM3 detected in prostate tissue microarray, specimens and cell lines were evaluated by immunohistochemistry and semi-quantitative PCR and Western blot, respectively. After being transfected with CMTM3 adenovirus or vector (mock), the proliferation and migration and invasion of LNCaP cells were detected by transwell assay and matrigel assay, respectively. Furthermore, the effects of CMTM3 on tumor growth were performed in nude mice xenograft in vivo. Results. We found CMTM3 was reduced in PCa tissues and cells compared with BPH tissues, and its expression in PCa tissues was related to the Gleason score. Moreover, after being transfected with adenovirus, ectopic expression of CMTM3 in LNCaP cells led to significant inhibition of cell proliferation and migration and invasion compared with the control (P < 0.05), which may be attributed to decreased Erk1/2 activity as p-Erk1/2 was remarkably reduced when CMTM3 was overexpressed. Finally, restoration of CMTM3 significantly suppressed xenograft tumor growth in vivo (P < 0.01) (AU)
RESUMEN
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Colección:
06-national
/
ES
Banco de datos:
IBECS
Asunto principal:
Neoplasias de la Próstata
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Terapia Genética
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Movimiento Celular
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Genes Supresores de Tumor
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Ensayos Antitumor por Modelo de Xenoinjerto
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Proliferación Celular
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Proteínas con Dominio MARVEL
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Clin. transl. oncol. (Print)
Año:
2015
Tipo del documento:
Article