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International braz j urol

Print version ISSN 1677-5538On-line version ISSN 1677-6119

Abstract

ZHANG, Caixiang et al. lncRNA CCAT1 promotes bladder cancer cell proliferation, migration and invasion. Int. braz j urol. [online]. 2019, vol.45, n.3, pp.549-559.  Epub June 27, 2019. ISSN 1677-6119.  https://doi.org/10.1590/s1677-5538.ibju.2018.0450.

Objective:

To study the expression patterns of long noncoding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) and the changes in cell proliferation, apoptosis, migration and invasion induced by silencing CCAT1 in bladder cancer cells.

Materials and Methods:

The expression levels of CCAT1 were determined using realtime quantitative polymerase chain reaction in cancerous tissues and paired normal tissues from 34 patients with bladder cancer. The relationship between clinical characteristics and CCAT1 expression was analyzed. And then we conducted cell experiments. Bladder urothelial carcinoma cell lines T24 and 5637 cells were transfected with CCAT1 small interfering RNA (siRNA) or scramble siRNA. Cell proliferation and apoptosis changes were determined using a Cell Counting Kit-8 (CCK-8) assay and a flow cytometry assay. Migration and invasion changes were measured using a wound healing assay and a trans-well assay. microRNAs (miRNAs) were predicted by Starbase 2.0, and their differential expression levels were studied.

Results:

CCAT1 was significantly upregulated in bladder cancer (P < 0.05). CCAT1 upregulation was positively related to tumor stage (P = 0.004), tumor grade (P = 0.001) and tumor size (P = 0.042). Cell proliferation, migration and invasion were promoted by abnormally expressed CCAT1. miRNAs miR-181b-5p, miR-152-3p, miR-24-3p, miR-148a-3p and miR-490-3p were potentially related to the aforementioned functions of CCAT1.

Conclusion:

CCAT1 plays an oncogenic role in urothelial carcinoma of the bladder. In addition, CCAT1 may be a potential therapeutic target in this cancer.

Keywords : Urinary Bladder Neoplasms; CCAT1 long noncoding RNA, human [Supplementary Concept]; Cell Proliferation.

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