Open Access

Long non‑coding RNA‑GAS5 acts as a tumor suppressor in bladder transitional cell carcinoma via regulation of chemokine (C‑C motif) ligand 1 expression

  • Authors:
    • Qifeng Cao
    • Ning Wang
    • Juan Qi
    • Zhengqin Gu
    • Haibo Shen
  • View Affiliations

  • Published online on: November 5, 2015     https://doi.org/10.3892/mmr.2015.4503
  • Pages: 27-34
  • Copyright: © Cao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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 GAS5 in order to silence or overexpress GAS5, respectively. The results of the present study demonstrated that knockdown of GAS5 expression promoted bladder cancer cell proliferation, whereas overexpression of GAS5 suppressed cell proliferation. Furthermore, knockdown of GAS5 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 GAS5, which may improve the ability of cells to regulate a stress response in vitro. Furthermore, knockdown of GAS5 expression increased the mRNA and protein expression of CCL1 in bladder cancer cells. Gain‑of‑function and loss‑of‑function studies demonstrated that GAS5 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 GAS5 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.
View Figures
View References

Related Articles

Journal Cover

January-2016
Volume 13 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Cao Q, Wang N, Qi J, Gu Z and Shen H: Long non‑coding RNA‑GAS5 acts as a tumor suppressor in bladder transitional cell carcinoma via regulation of chemokine (C‑C motif) ligand 1 expression. Mol Med Rep 13: 27-34, 2016
APA
Cao, Q., Wang, N., Qi, J., Gu, Z., & Shen, H. (2016). Long non‑coding RNA‑GAS5 acts as a tumor suppressor in bladder transitional cell carcinoma via regulation of chemokine (C‑C motif) ligand 1 expression. Molecular Medicine Reports, 13, 27-34. https://doi.org/10.3892/mmr.2015.4503
MLA
Cao, Q., Wang, N., Qi, J., Gu, Z., Shen, H."Long non‑coding RNA‑GAS5 acts as a tumor suppressor in bladder transitional cell carcinoma via regulation of chemokine (C‑C motif) ligand 1 expression". Molecular Medicine Reports 13.1 (2016): 27-34.
Chicago
Cao, Q., Wang, N., Qi, J., Gu, Z., Shen, H."Long non‑coding RNA‑GAS5 acts as a tumor suppressor in bladder transitional cell carcinoma via regulation of chemokine (C‑C motif) ligand 1 expression". Molecular Medicine Reports 13, no. 1 (2016): 27-34. https://doi.org/10.3892/mmr.2015.4503