@Article{096504017X15000757094686,
AUTHOR = {Dong Yang, Jian-Jun Wang, Jin-Song Li, Qian-Yu Xu},
TITLE = {miR-103 Functions as a Tumor Suppressor by Directly Targeting  Programmed Cell Death 10 in NSCLC},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {4},
PAGES = {519--528},
URL = {http://www.techscience.com/or/v26n4/56664},
ISSN = {1555-3906},
ABSTRACT = {Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. Absence of miR-103 
has recently been identified to be associated with metastatic capacity of primary lung tumors. However, the 
exact role of miR-103 in NSCLC and the molecular mechanism are unclear. In the present study, we showed 
that miR-103 expression was reduced in NSCLC tissues and cells. miR-103 expression was negatively correlated with tumor size and stage. The overall survival was longer in patients with higher miR-103 level than 
in those with lower miR-103 expression. miR-103 inhibited cell proliferation in A549 cells, decreased tumor 
weight and volume, and prolonged survival of tumor-implanted nude mice. miR-103 increased apoptotic cell 
death in A549 cells. Furthermore, miR-103 decreased the invasion and migration abilities in A549 cells, as 
evidenced by Transwell and wound healing results. Downregulation of miR-103 significantly reduced the level 
of programmed cell death 10 (PDCD10). We found a significant decrease in the relative luciferase activity 
of the reporter gene in A549 cells cotransfected with the miR-103 mimic and pGL3-PDCD10 WT 3'-UTR, 
but not pGL3-PDCD10 mut 3'-UTR. We showed that overexpression of PDCD10 significantly inhibited 
miR-103-induced inhibition of cell proliferation, increased apoptosis, and decreased invasion and migration in 
A549 cells. Moreover, we found that PDCD10 expression was increased in NSCLC tissues and cells. PDCD10 
expression was positively correlated with tumor size and stage. Overexpression of PDCD10 increased cell 
proliferation and inhibited apoptosis in A549 cells. The data demonstrated that dysregulation of the miR-103/
PDCD10 signal may be a novel therapeutic target for the treatment of NSCLC.},
DOI = {10.3727/096504017X15000757094686}
}