@Article{096504017X14878518291077,
AUTHOR = {Boda Ying, Hong Huang, Hongfei Li, Meng Song, Sizhan Wu, Hongliang Ying},
TITLE = {Procaine Inhibits Proliferation and Migration and Promotes Cell Apoptosis in  Osteosarcoma Cells by Upregulation of MicroRNA-133b},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {9},
PAGES = {1463--1470},
URL = {http://www.techscience.com/or/v25n9/56931},
ISSN = {1555-3906},
ABSTRACT = {Procaine (PCA) is a conventional chemotherapeutic agent for osteosarcoma. Recent studies have proposed 
that the growth-inhibitory effect of PCA is through regulation of microRNAs (miRNAs). miR-133b has been 
proven to be a tumor suppressor in osteosarcoma, but whether it is involved in the antitumor effects of PCA on 
osteosarcoma has not been investigated. In this study, we aimed to explore the effects of PCA on osteosarcoma 
MG63 cells by regulation of miR-133b, as well as its underlying mechanisms. MG63 cells were treated with 
different concentrations of PCA, and cell viability, apoptosis, and miR-133b expression were then detected 
by MTT, flow cytometry, and qRT-PCR, respectively. Cells were then transfected with the miR-133b inhibitor and treated with 2 µM PCA. Thereafter, cell viability, migration, and apoptosis were detected. Analysis of 
signaling pathways was detected by Western blot. Our results showed that PCA significantly inhibited cell 
viability and promoted apoptosis and the expression level of miR-133b in a dose-dependent manner (<i>p</i>< 0.05 
or <i>p</i><0.01). Moreover, we observed that PCA + miR-133b inhibitor dramatically reversed the effects of PCA on 
cell viability, apoptosis, and migration (<i>p</i><0.05 or <i>p</i><0.01). In addition, PCA significantly decreased the levels 
of p/t-AKT (p308 or p473), p/t-ERK, and p/t-S6, whereas PCA + miR-133b inhibitor rescued these effects. Our 
results suggest that PCA inhibits proliferation and migration but promotes apoptosis in osteosarcoma cells by 
upregulation of miR-133b. These effects may be achieved by inactivation of the AKT/ERK pathways.},
DOI = {10.3727/096504017X14878518291077}
}