@Article{096504018X15172747209020,
AUTHOR = {Feng Shuai, Bo Wang, Shuxiao Dong},
TITLE = {MicroRNA-204 Inhibits the Growth and Motility of Colorectal  Cancer Cells by Downregulation of CXCL8},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {8},
PAGES = {1295--1305},
URL = {http://www.techscience.com/or/v26n8/56759},
ISSN = {1555-3906},
ABSTRACT = {Among all of the miRNAs, miR-204 has gained considerable attention in the field of cancer research. This 
study aimed to reveal the detailed functions and the underlying mechanism of miR-204 in colorectal cancer 
(CRC) cells. The expressions of miR-204 in CRC tumor tissues and cell lines were monitored. Expressions 
of miR-204 and CXCL8 in Caco-2 and HT-29 cells were altered by transfection, and then cell viability, apoptosis, migration, invasion, EMT-related protein expression, and PI3K/AKT/mTOR pathway protein expression were assessed. We found that miR-204 was expressed at low levels in CRC tumor tissues and cell lines 
when compared to their normal controls. miR-204 overexpression reduced the viability, migration, and invasion of Caco-2 and HT-29 cells while significantly inducing apoptosis. miR-204 overexpression upregulated 
E-cadherin expression and downregulated N-cadherin and vimentin expressions. CXCL8 was a target of 
miR-204, and miR-204 suppression could not increase cell viability, migration, invasion, and EMT procedure 
when CXCL8 was silenced. Moreover, miR-204 overexpression decreased the phosphorylated levels of PI3K, 
AKT, and mTOR. The increased phosphorylations of PI3K, AKT, and mTOR, and the upregulation of CXCL8 
induced by miR-204 suppression were all abolished by the addition of LY294002 and AZD8055 (inhibitors 
of PI3K/AKT and mTOR, respectively). To conclude, we demonstrated a tumor-suppressive miRNA in CRC 
cell lines, miR-204, which is poorly expressed in CRC tissues and cell lines. miR-204 exerted antigrowth, 
antimigration, anti-invasion, and anti-EMT activities, which might be via deactivating the PI3K/AKT/mTOR 
pathway and repressing CXCL8 expression.},
DOI = {10.3727/096504018X15172747209020}
}