Startseite Lebenswissenschaften LncRNA PART1 modulates toll-like receptor pathways to influence cell proliferation and apoptosis in prostate cancer cells
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LncRNA PART1 modulates toll-like receptor pathways to influence cell proliferation and apoptosis in prostate cancer cells

  • Ming Sun , Donghua Geng , Shuqiang Li , Zhaofu Chen und Wenyan Zhao EMAIL logo
Veröffentlicht/Copyright: 20. Dezember 2017

Abstract

We investigated thoroughly the effect of lncRNA PART1 on prostate cancer cells proliferation and apoptosis, through regulating toll-like receptor (TLR) pathways. LncRNA PART1 expression was also examined by quantitative real-time polymerase chain reactions (qRT-PCR) in human tissues and the cells lines LNCaP and PC3. After transfection with si-PART1 or control constructs, the cell viability was measured by MTS and colony formation assays. In addition, the apoptosis rate of the prostate cancer cells was validated by TUNEL staining. Relationships between lncRNA PART1 expression and TLR pathway genes were demonstrated by qRT-PCR and Western blotting. High levels of lncRNA PART1 expression were correlated with advanced cancer stage and predication of poor survival. LncRNA PART1 levels was increased in PCa cells treated with 5α-dihydrotestosterone (DHT), confirming PART1 was directly induced by androgen. Moreover, down-regulation of lncRNA PART1 inhibited prostate cancer cell proliferation and accelerated cell apoptosis. In addition, lncRNA PART1 induced downstream genes expression in TLR pathways including TLR3, TNFSF10 and CXCL13 to further influence prostate cancer cells, indicating its carcinogenesis on prostate cancer. LncRNA PART1 promoted cell proliferation ability and apoptosis via the inhibition of TLR pathways in prostate cancer. LncRNA PART1 could hence be considered as a new target in the treatment of prostate cancer.

Acknowledgments

We would like to acknowledge the reviewers for their helpful comments on this paper.

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Supplemental Material:

The online version of this article offers supplementary material (https://doi.org/10.1515/hsz-2017-0255).


Received: 2017-9-29
Accepted: 2017-12-1
Published Online: 2017-12-20
Published in Print: 2018-3-28

©2018 Walter de Gruyter GmbH, Berlin/Boston

Heruntergeladen am 10.12.2025 von https://www.degruyterbrill.com/document/doi/10.1515/hsz-2017-0255/pdf
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