Journal
MOLECULAR MEDICINE REPORTS
Volume 13, Issue 1, Pages 27-34Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2015.4503
Keywords
growth arrest-specific 5; chemokine (C-C motif) ligand 1; long non-coding RNA; bladder cancer
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Long non-coding RNAs (lncRNAs) have important roles in diverse biological processes, including transcriptional regulation, cell growth and tumorigenesis. The present study aimed to investigate whether lncRNA-growth arrest-specific (GAS)5 regulated bladder cancer progression via regulation of chemokine (C-C) ligand (CCL)1 expression. The viability of BLX bladder cancer cells was detected using a Cell Counting kit-8 assay, and cell apoptosis was assessed by annexin V-propidium iodide double-staining. The expression levels of specific genes and proteins were analyzed by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. In addition, cells were transfected with small interfering (si)RNAs or recombinant GASS in order to silence or overexpress GASS, respectively. The results of the present study demonstrated that knockdown of GASS expression promoted bladder cancer cell proliferation, whereas overexpression of GAS5 suppressed cell proliferation. Furthermore, knockdown of GASS resulted in an increased percentage of cells in S and G2 phase, and a decreased percentage of cells in G1 phase. In addition, the present study performed a hierarchical cluster analysis of differentially expressed lncRNAs in bladder cancer cells and detected that CCL1 overexpression resulted in an upregulation of GASS, which may improve the ability of cells to regulate a stress response in vitro. Furthermore, knockdown of GASS expression increased the mRNA and protein expression of CCL1 in bladder cancer cells. Gain-of-function and loss-of-function studies demonstrated that GASS was able to inhibit bladder cancer cell proliferation, at least in part, by suppressing the expression of CCL1. The results of the present study demonstrated that GASS was able to suppress bladder cancer cell proliferation, at least partially, by suppressing the expression of CCL1. The results of the present study may provide a basis for developing novel effective treatment strategies against bladder cancer.
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