Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27347346
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Overexpression of long non-coding RNA HOTTIP increases chemoresistance of
osteosarcoma cell by activating the Wnt/?-catenin pathway
#MMPMID27347346
Li Z
; Zhao L
; Wang Q
Am J Transl Res
2016[]; 8
(5
): 2385-93
PMID27347346
show ga
Long non-coding RNAs (lncRNAs) have been identified as oncogenes or tumor
suppressors that are involved in tumorigenesis and chemotherapy resistance.
HOTTIP is located at the 5' tip of the HOXA locus and coordinates the activation
of multiple 5' HOXA genes, which plays an important role in multiple cancers.
However, its biological role in the development of the chemoresistance phenotype
of osteosarcoma (OS) is still unknown. In this study, we explored the roles of
lncRNA HOTTIP in the initiation and chemoresistance of OS. We found that HOTTIP
was increased in OS and up-regulated expression of HOTTIP could promoted OS cell
proliferation and cell cycle progression by activating the Wnt/?-catenin pathway.
Down-regulated expression of HOTTIP inhibited cell proliferation and arrested
cell cycle at G1 phase by inhibition of Wnt/?-catenin pathway. Furthermore, our
data showed that increased expression of HOTTIP was correlated with
chemoresistance in OS. In vitro, HOTTIP induced cellular resistance to cisplatin
by activating the Wnt/?-catenin pathway, which could be reversed by treatment
with the Wnt/?-catenin inhibitor. Taken together, these findings indicated that
HOTTIP play a pivotal role in OS cell initiation and chemoresistance via
activating Wnt/?-catenin signaling pathway, which suggested potential use of
HOTTIP for the treatment of osteosarcoma.
free
free
free
