
@Article{096504017X14944585873631,
AUTHOR = {Ye Li, Haihong Luo, Nan Xiao, Jianmin Duan, Zhiping Wang, Shuanke Wang},
TITLE = {Long Noncoding RNA SChLAP1 Accelerates the Proliferation and Metastasis of  Prostate Cancer via Targeting miR-198 and Promoting the MAPK1 Pathway},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {1},
PAGES = {131--143},
URL = {http://www.techscience.com/or/v26n1/56625},
ISSN = {1555-3906},
ABSTRACT = {Prostate cancer has become the most commonly diagnosed and the second leading cause of cancer-related 
deaths in males. The long noncoding RNA second chromosome locus associated with prostate-1 (SChLAP1) 
has been found to be overexpressed in a subset of prostate cancer. However, the significance and mechanism 
of SChLAP1 in prostate cancer are not well known. In this study, we explored the role of SChLAP1 in prostate 
cancer tissues, cell lines, and mouse models. The effect of SChLAP1 on miR-198 and MAPK1 was specifically 
examined. We found that SChLAP1 expression was significantly increased in prostate cancer cells and tissues. 
Knockdown of SChLAP1 promoted apoptosis and inhibited cell proliferation and invasion in vitro and in vivo. 
In addition, a potential bonding site between miR-198 and SChLAP1 was predicted, and a low expression of 
miR-198 was found in prostate cancer tissues and cells. Knockdown of SChLAP1 significantly increased the 
expression of miR-198, and SChLAP1 overexpression markedly decreased it, indicating that SChLAP1 acted 
as a negative regulator in the expression of miR-198. Furthermore, our results showed that SChLAP1 interacted 
with miR-198 and subsequently modulated the MAPK1 signaling pathway in prostate cancer. In conclusion, 
our study has identified a novel pathway through which SChLAP1 exerts its oncogenic role in prostate cancer 
at the level of miRNAs and provided a molecular basis for potential applications of SChLAP1 in the prognosis 
and treatment of prostate cancer.},
DOI = {10.3727/096504017X14944585873631}
}



