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Table S2 from LncRNA CCAT1 Promotes Prostate Cancer Cell Proliferation by Interacting with DDX5 and MIR-28-5P

dataset

posted on 2023-04-03, 15:22 authored by Zonghao You, Chunhui Liu, Can Wang, Zhixin Ling, Yiduo Wang, Yali Wang, Minghao Zhang, Shuqiu Chen, Bin Xu, Han Guan, Ming Chen

The list of miRNAs pulled down by CCAT1 sense and antisense strand in our RNA pulldown assay.

Funding

National Natural Science Foundation of China

Natural Science Foundation of Jiangsu Province

History

ARTICLE 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.