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Article

Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901

  • Authors:
    • Xiao‑Min Chen
    • Jun‑Ming Guo
    • Ping Chen
    • Lian‑Gang Mao
    • Wei‑Yun Feng
    • Dong‑Hai Le
    • Ke‑Qiang Li
  • View Affiliations / Copyright

    Affiliations: Ningbo University School of Medicine, Ningbo, Zhejiang 315211, P.R. China, Oncomolecularbiology Laboratory of Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, P.R. China
  • Pages: 2327-2333
    |
    Published online on: August 28, 2014
       https://doi.org/10.3892/mmr.2014.2523
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Abstract

Scinderin is a Ca2+‑dependent filamentous actin (F‑actin) severing and capping protein, which has a key role in regulated secretion. However, little is known regarding the function and mechanism of scinderin in human carcinoma development and progression. In the present study, the biological function of scinderin was investigated using a cell proliferation assay, flow cytometric analysis and a Transwell assay in highly tumorigenic and the metastatic human gastric cancer cell line SGC‑7901 transfected with scinderin‑small hairpin RNA lentivirus. The changes in the expression of epithelial‑mesenchymal transition (EMT) markers were also investigated. The results indicated that scinderin knockdown effectively suppressed proliferation, reduced migration and arrested the cell cycle of the SGC‑7901 cells at G2/M phase. Furthermore, scinderin knockdown altered the expression of EMT markers; the expression of E‑cadherin was significantly upregulated, along with an evident decrease in N‑cadherin and β‑catenin expression. In conclusion, the present study suggested that suppression of scinderin impaired proliferation and migration of gastric cancer SGC‑7901 cells and attenuates its EMT process. Scinderin may therefore be a potential target for tumor EMT and therapy against gastric cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Chen XM, Guo JM, Chen P, Mao LG, Feng WY, Le DH and Li KQ: Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901. Mol Med Rep 10: 2327-2333, 2014.
APA
Chen, X., Guo, J., Chen, P., Mao, L., Feng, W., Le, D., & Li, K. (2014). Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901. Molecular Medicine Reports, 10, 2327-2333. https://doi.org/10.3892/mmr.2014.2523
MLA
Chen, X., Guo, J., Chen, P., Mao, L., Feng, W., Le, D., Li, K."Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901". Molecular Medicine Reports 10.5 (2014): 2327-2333.
Chicago
Chen, X., Guo, J., Chen, P., Mao, L., Feng, W., Le, D., Li, K."Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901". Molecular Medicine Reports 10, no. 5 (2014): 2327-2333. https://doi.org/10.3892/mmr.2014.2523
Copy and paste a formatted citation
x
Spandidos Publications style
Chen XM, Guo JM, Chen P, Mao LG, Feng WY, Le DH and Li KQ: Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901. Mol Med Rep 10: 2327-2333, 2014.
APA
Chen, X., Guo, J., Chen, P., Mao, L., Feng, W., Le, D., & Li, K. (2014). Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901. Molecular Medicine Reports, 10, 2327-2333. https://doi.org/10.3892/mmr.2014.2523
MLA
Chen, X., Guo, J., Chen, P., Mao, L., Feng, W., Le, D., Li, K."Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901". Molecular Medicine Reports 10.5 (2014): 2327-2333.
Chicago
Chen, X., Guo, J., Chen, P., Mao, L., Feng, W., Le, D., Li, K."Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901". Molecular Medicine Reports 10, no. 5 (2014): 2327-2333. https://doi.org/10.3892/mmr.2014.2523
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