Effects of Slit3 silencing on the invasive ability of lung carcinoma A549 cells

  • Authors:
    • Chao Zhang
    • Hui Guo
    • Bin Li
    • Chengzhi Sui
    • Yuan Zhang
    • Xianyuan Xia
    • Ying Qin
    • Liying Ye
    • Fu'an Xie
    • Heng Wang
    • Mingjing Yuan
    • Li Yuan
    • Jun Ye
  • View Affiliations

  • Published online on: June 5, 2015     https://doi.org/10.3892/or.2015.4031
  • Pages: 952-960
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Slit proteins function as chemorepellents in axon guidance and neuronal migration by binding to cognate Robo receptors. The Slit/Robo signaling pathway is also involved in the regulation of tumor cell metastasis. However, whether the Slit/Robo signaling pathway exerts prometastatic or antimetastasis functions remains controversial. To date, most of the research on Slit/Robo has focused on Slit2, and the effects of Slit3 on metastasis remain largely unknown. Based on the Oncomine database, overall expression of Slit3 is low in tumor tissues compared to its level in normal tissues. The underlying mechanism for slit3 silencing in tumor tissues is likely related to hypermethylation of the slit3 promoter. However, lung carcinomas appear to be an exception. Several studies have reported that the frequency of Slit3 methylation in lung cancers is far lower than the frequency of Slit2. In the present study, high Slit3 expression at the mRNA level, yet not at the protein level, was detected in lung adenocarcinoma A549 cells. The function of Slit3 in tumor migration and invasion was examined by silencing of Slit3 expression in A549 cells. Silencing of Slit3 promoted proliferation, migration and invasion of A549 cells and induced epithelial-mesenchymal transition by downregulation of E-cadherin and upregulation of vimentin. The inhibitory effects of Slit3 on tumor migration and invasion are likely related to matrix metalloproteinases (MMPs). Silencing of Slit3 in the A549 cells enhanced MMP2 and MMP9 expression. These results indicate that Slit3 is a potential tumor suppressor in lung adenocarcinoma.
View Figures
View References

Related Articles

Journal Cover

August-2015
Volume 34 Issue 2

Print ISSN: 1021-335X
Online ISSN:1791-2431

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhang C, Guo H, Li B, Sui C, Zhang Y, Xia X, Qin Y, Ye L, Xie F, Wang H, Wang H, et al: Effects of Slit3 silencing on the invasive ability of lung carcinoma A549 cells. Oncol Rep 34: 952-960, 2015
APA
Zhang, C., Guo, H., Li, B., Sui, C., Zhang, Y., Xia, X. ... Ye, J. (2015). Effects of Slit3 silencing on the invasive ability of lung carcinoma A549 cells. Oncology Reports, 34, 952-960. https://doi.org/10.3892/or.2015.4031
MLA
Zhang, C., Guo, H., Li, B., Sui, C., Zhang, Y., Xia, X., Qin, Y., Ye, L., Xie, F., Wang, H., Yuan, M., Yuan, L., Ye, J."Effects of Slit3 silencing on the invasive ability of lung carcinoma A549 cells". Oncology Reports 34.2 (2015): 952-960.
Chicago
Zhang, C., Guo, H., Li, B., Sui, C., Zhang, Y., Xia, X., Qin, Y., Ye, L., Xie, F., Wang, H., Yuan, M., Yuan, L., Ye, J."Effects of Slit3 silencing on the invasive ability of lung carcinoma A549 cells". Oncology Reports 34, no. 2 (2015): 952-960. https://doi.org/10.3892/or.2015.4031