HCP5 promotes colon cancer development by activating AP1G1 via PI3K/AKT pathway.
Eur Rev Med Pharmacol Sci
; 23(7): 2786-2793, 2019 Apr.
Article
em En
| MEDLINE
| ID: mdl-31002129
ABSTRACT
OBJECTIVE:
To explore whether HCP5 participates in the pathogenic progression of colon cancer (CC) and its underlying mechanism. PATIENTS ANDMETHODS:
HCP5 expression in CC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between the HCP5 expression and tumor stage of CC patients was then analyzed. After CC cells were transfected with HCP5-siRNA, the proliferation and migration capacities were detected by cell counting kit-8 (CCK-8), colony formation and transwell assay, respectively. Cell cycle was examined by flow cytometry. Western blot was conducted to detect protein expressions of HCP5, AP1G1 and relative molecules in the PI3K/AKT pathway. Rescue experiments were performed by co-transfection of HCP5-siRNA and AP1G1-siRNA into CC cells, followed by cell function detection.RESULTS:
HCP5 was highly expressed, whereas AP1G1 was lowly expressed in CC tissues and cell lines. Besides, CC patients with stage III-IV presented higher expression of HCP5 than those with stage I-II. The knockdown of HCP5 in CC cells down-regulated proliferation and migration capacities, and arrested cell cycle in the G0/G1 phase, which was reversed by the AP1G1 knockdown. In addition, HCP5 knockdown up-regulated AP1G1 expression, whereas down-regulated the expression of relative proteins in the PI3K/AKT pathway.CONCLUSIONS:
HCP5 was significantly increased in CC and enhanced the proliferation and migration of CC cells by inhibiting the AP1G1 expression. HCP5 promoted CC development by activating the PI3K/AKT pathway.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias do Colo
/
Complexo 1 de Proteínas Adaptadoras
/
RNA Longo não Codificante
Tipo de estudo:
Incidence_studies
/
Prognostic_studies
Limite:
Humans
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article