Expression of CHPF modulates cell proliferation and invasion in lung cancer
Braz. j. med. biol. res
;
53(5): e9021, 2020. graf
Artículo
en Inglés
| LILACS
| ID: biblio-1098108
ABSTRACT
Lung cancer is the most common malignancy worldwide and is characterized by rapid progression, aggressive behavior, frequent recurrence, and poor prognosis. The TCGA database indicates that chondroitin polymerizing factor (CHPF) is overexpressed in human lung cancer tissues compared with normal tissues and this overexpression corresponds to shorter overall survival in lung cancer patients. In this study, to investigate the function of CHPF in lung cancer, lentiviral vectors expressing CHPF shRNA were stably transduced into A549 and H1299 cells. Compared to shCtrl cells, CHPF knockdown cells had significantly reduced proliferation. Furthermore, the silencing of CHPF in A549 and H1299 cells resulted in apoptotic induction, which led to decreased colony formation. Wound healing and transwell invasion assays revealed that CHPF could positively regulate the migration of lung cancer cells. The tumorigenic role of CHPF was also validated in nude mouse xenograft models. Affymetrix gene chip analysis indicated that CHPF regulated the proliferation and invasion of lung cancer cells through CDH1, RRM2, MKI67, and TNFRSF10B. We thus highlight CHPF as a novel target for lung cancer treatment.
Texto completo:
Disponible
Índice:
LILACS (Américas)
Asunto principal:
Regulación Neoplásica de la Expresión Génica
/
N-Acetilgalactosaminiltransferasas
/
Neoplasias Pulmonares
Tipo de estudio:
Estudio pronóstico
Límite:
Animales
/
Femenino
/
Humanos
Idioma:
Inglés
Revista:
Braz. j. med. biol. res
Asunto de la revista:
Biologia
/
Medicina
Año:
2020
Tipo del documento:
Artículo
País de afiliación:
China
Institución/País de afiliación:
Nanjing Medical University/CN
/
Xuzhou Center Hospital/CN
/
Xuzhou Medical University/CN
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