Knockdown of Mgat5 inhibits CD133+ human pulmonary adenocarcinoma cell growth in vitro and in vivo.
Clin Invest Med
; 34(3): E155-62, 2011 Jun 01.
Article
en En
| MEDLINE
| ID: mdl-21631992
ABSTRACT
PURPOSE:
In spite of many therapeutic advances, the prognosis of lung cancer remains poor. Therefore, understanding the molecular mechanisms underlying cancer progression, invasion and metastasis is needed. Accumulating evidence indicate that N-acetylglucosaminyltransferase V (Mgat5 or GnT-V) is involved in cancer development. The purpose of this study was to characterize the expression and function of Mgat5 in CD133+ pulmonary adenocarcinoma cells.METHODS:
CD133+ pulmonary adenocarcinoma cells were separated by magnetic activated cell sorting (MACS) from excised pulmonary adenocarcinoma specimens from 10 patients. Expression of Mgat5 in CD133+ cells was detected by fluorescent quantitative RT-PCR (FQRT-PCR) and Western blot. Subsequently, CD133+ cells were transfected with specific siRNA of Mgat5 to evaluate the effects of Mgat5 inhibition on cancer cell growth in vivo and in vitro.RESULTS:
Expression of Mgat5 was 1.2-fold and 1.4-fold higher in CD133+cells than in CD133- cells detected by FQRT-PCR and Western Blot, respectively (p < 0.05). The L-PHA binding assay also showed higher reactivity in CD133+ cells than in CD133- cells. In addition, Mgat5-specific siRNA efficiently knocked down the expression of Mgat5 in CD133+ cells. Interestingly, downregulation of Mgat5 resulted in significant inhibition of cancer cell growth in vitro and in vivo.CONCLUSION:
Mgat5 is expressed at a relatively high level in CD133+ lung adenocarcinoma cells, and knockdown of Mgat5 in CD133+ cells inhibits cancer cell growth both in vitro and in vivo. These findings suggest Mgat5 may play an important role during oncogenesis, identifying a potential therapeutic target for pulmonary adenocarcinoma.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Péptidos
/
Glicoproteínas
/
Adenocarcinoma
/
Antígenos CD
/
N-Acetilglucosaminiltransferasas
/
Neoplasias Pulmonares
Tipo de estudio:
Prognostic_studies
Límite:
Animals
/
Female
/
Humans
/
Male
Idioma:
En
Revista:
Clin Invest Med
Año:
2011
Tipo del documento:
Article