LncRNA CCAT1 Promotes Prostate Cancer Cell Proliferation by Interacting with DDX5 and MIR-28-5P.

Abstract:

:Accumulated evidence indicates that CCAT1 functions as an oncogene in the progression of a variety of tumors. However, little is known as to how CCAT1 impacts tumorigenesis in human prostate cancer. In this study, we found from The Cancer Genome Atlas and Memorial Sloan Kettering Cancer Center database that CCAT1 is highly upregulated in castration-resistant prostate cancer (CRPC) compared with androgen-dependent prostate cancer (ADPC). Higher level of CCAT1 leads to increased mortality in patients with CRPC. In vitro and in vivo studies show that CCAT1 promotes prostate cancer cell proliferation as well as the tumor growth of prostate cancer xenografts. Mechanistically, in cytoplasm, CCAT1 sponges MIR-28-5P to prevent the anticancer effect. In nucleus, CCAT1 acts as a scaffold for DDX5 (P68) and AR transcriptional complex to facilitate the expression of AR-regulated genes, thus stimulating CRPC progression. Our findings suggest that CCAT1 is an oncogenic factor in the progression of CRPC with different regulatory mechanisms in the nucleus and cytoplasm of cells.

journal_name

Mol Cancer Ther

authors

You Z,Liu C,Wang C,Ling Z,Wang Y,Wang Y,Zhang M,Chen S,Xu B,Guan H,Chen M

doi

10.1158/1535-7163.MCT-19-0095

subject

Has Abstract

pub_date

2019-12-01 00:00:00

pages

2469-2479

issue

12

eissn

1535-7163

issn

1538-8514

pii

1535-7163.MCT-19-0095

journal_volume

18

pub_type

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