Long non-coding RNA PCAT-1 contributes to tumorigenesis by regulating FSCN1 via miR-145-5p in prostate cancer

Prostate cancer associated lncRNA transcript 1 (PCAT-1) has been identified as an oncogenic long non-coding RNA (lncRNA) in some solid tumors, including prostate cancer (PC). However, the molecular mechanism of PCAT-1 involved in PC is poorly defined. In this study, we found that PCAT-1 expression w...

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Bibliographic Details
Published in:Biomedicine & pharmacotherapy 2017-11, Vol.95, p.1112-1118
Main Authors: Xu, Weibo, Chang, Junkai, Du, Xinyi, Hou, Junqing
Format: Article
Language:English
Subjects:
Apoptosis - genetics
Base Sequence
Carcinogenesis - genetics
Carrier Proteins - genetics
Carrier Proteins - metabolism
Caspase 3 - metabolism
Cell Line, Tumor
Cell Movement - genetics
Cell Proliferation - genetics
Disease Progression
FSCN1
Gene Expression Regulation, Neoplastic
Humans
lncRNA PCAT-1
Male
Microfilament Proteins - genetics
Microfilament Proteins - metabolism
MicroRNAs - genetics
MicroRNAs - metabolism
miR-145-5p
Neoplasm Invasiveness
Prostate cancer
Prostatic Neoplasms - enzymology
Prostatic Neoplasms - genetics
Prostatic Neoplasms - pathology
Reproducibility of Results
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
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Summary:Prostate cancer associated lncRNA transcript 1 (PCAT-1) has been identified as an oncogenic long non-coding RNA (lncRNA) in some solid tumors, including prostate cancer (PC). However, the molecular mechanism of PCAT-1 involved in PC is poorly defined. In this study, we found that PCAT-1 expression was up-regulated and miR-145-5p expression was down-regulated in PC tissues and cells. Function analysis indicated that PCAT-1 overexpression promoted proliferation, migration, invasion and inhibited apoptosis of PC cells. Rescue experiments demonstrated that miR-145-5p restoration attenuated the promotive effects of PCAT1 on PC progression, while Fascin-1 (FSCN1) upregulation relieved the anti-cancer role of miR-145-5p in PC. Mechanical analysis discovered that PCAT-1 could act as a miR-145-5p sponge to modulate FSCN1 expression. In conclusion, these findings suggested that PCAT-1 accelerated PC cell proliferation, migration, invasion and suppressed apoptosis by up-regulating FSCN1 mediated via miR-145-5p, hinting a potential therapeutic strategy for PC patients.
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2017.09.019