Abstract
Long non-coding RNAs (lncRNAs) play important roles in diverse biological processes, such as transcriptional regulation, cell growth and tumorigenesis. However, little is known about whether lncRNA-GAS5 (growth arrest-specific 5) regulates bladder cancer progression. In the present study, we found that the GAS5 expression is commonly downregulated in bladder cancer cell lines and human specimens. Knockdown of GAS5 promotes bladder cancer cell proliferation, whereas forced expression of GAS5 suppresses cell proliferation. We further demonstrated that knockdown of GAS5 increases CDK6 mRNA and protein levels in bladder cancer cells. Expectedly, GAS5 inhibition induces a significant decrease in G0/G1 phase and an obvious increase in S phase. Gain-of-function and loss-of-function studies showed that GAS5 inhibits bladder cancer cell proliferation, at least in part, by regulating CDK6 expression.ConclusionsDownregulated GAS5 promotes bladder cancer cell proliferation, partly by regulating CDK6, and thus may be helpful in the development of effective treatment strategies against bladder cancer.
Highlights
Human bladder cancer is the fourth most common malignancy in men, and the tenth most common in women [1,2]
Real-time Polymerase Chain Reaction (PCR) was carried out using a standard protocol from the SYBR Green PCR kit (Toyobo, Osaka, Japan) on Applied Biosystems 7300 Real Time PCR system (Applied Biosystems, Foster City, CA) according to the instructions. b-actin was used as references for Long non-coding RNAs (lncRNAs)
In order to investigate whether GAS5 regulates bladder tumorigenesis, we first examined the GAS5 expression level in bladder cancer tissues and adjacent normal tissues
Summary
Human bladder cancer is the fourth most common malignancy in men, and the tenth most common in women [1,2]. The most common histological type of bladder cancer is urothelial carcinoma (UC) which are non-invasive papillary tumors that commonly recur but rarely progress [3]. Invasive bladder tumors are more aggressive, and patients with muscle invasive UC are usually treated with radical cystectomy. One-half of patients with invasive bladder cancer develop subsequent metastatic disease, even after radical surgery of the primary tumors [6]. The advances in effective therapy for bladder cancer have been limited because the pathological mechanisms causing tumor are not known. Revealing the molecular mechanism for the bladder tumorigenesis is indispensable for developing effective treatment
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