Open Access

Suppression of A549 cell proliferation and metastasis by calycosin via inhibition of the PKC‑α/ERK1/2 pathway: An in vitro investigation

Corrigendum in: /10.3892/mmr.2016.4976

  • Authors:
    • Xu‑Dong Cheng
    • Jun‑Fei Gu
    • Jia‑Rui Yuan
    • Liang Feng
    • Xiao‑Bin Jia
  • View Affiliations

  • Published online on: October 15, 2015     https://doi.org/10.3892/mmr.2015.4449
  • Pages: 7992-8002
  • Copyright: © Cheng 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

The migration and invasion of lung cancer cells into the extracellular matrix contributes to the high mortality rates of lung cancer. The protein kinase C (PKC) and downstream signaling pathways are important in the invasion and migration of lung cancer cells. Calycosin (Cal), an effector chemical from Astragalus has been reported to affect the recurrence and metastasis of cancer cells via the regulation of the protein expression of matrix metalloproteinases (MMPs). The inhibition of Cal on the migration and invasion of A549 cells was investigated in the present study. Cell viability and apoptosis assays were performed using MTT and flow cytometric analyses. A wound healing assay and Transwell invasion assay were performed to evaluate the effect of Cal on A549 cell migration and invasion. Invasion‑associated proteins, including MMP‑2, MMP‑9, E‑cadherin (E‑cad), integrin β1, PKC‑α and extracellular signal‑regulated kinase 1/2 (ERK1/2) were detected using western blotting. In addition, PKC‑α inhibitor, AEB071, and ERK1/2 inhibitor, PD98059, were used to determine the association between the suppression of PKC‑α /ERK1/2 and invasion, MMP‑2, MMP‑9, E‑cad and integrin β1. Cal was observed to suppress cell proliferation and induce apoptosis. There were significant differences between the phorbol‑12‑myristate‑13‑acetate (TPA)‑induced A549 cells treated with Cal and the untreated cells in the rates of migration and invasion. The levels of MMP‑2, MMP‑9, E‑cad and integrin β1 in the TPA‑induced A549 cells changed markedly, compared with the untreated cells. In addition, the suppression of Cal was affected by the PKC inhibitor, AEB071, an ERK1/2 inhibitor, PD98059. The results of the present study indicated that Cal inhibited the proliferation, adhesion, migration and invasion of the TPA‑induced A549 cells. The Cal‑induced repression of PKC‑α/ERK1/2, increased the expression of E‑Cad and inhibited the expression levels of MMP‑2, MMP‑9 and integrin β1, which possibly demonstrates the mechanism underlying the biological anticancer effects of Cal.
View Figures
View References

Related Articles

Journal Cover

December-2015
Volume 12 Issue 6

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
Cheng XD, Gu JF, Yuan JR, Feng L and Jia XB: Suppression of A549 cell proliferation and metastasis by calycosin via inhibition of the PKC‑α/ERK1/2 pathway: An in vitro investigation Corrigendum in /10.3892/mmr.2016.4976. Mol Med Rep 12: 7992-8002, 2015
APA
Cheng, X., Gu, J., Yuan, J., Feng, L., & Jia, X. (2015). Suppression of A549 cell proliferation and metastasis by calycosin via inhibition of the PKC‑α/ERK1/2 pathway: An in vitro investigation Corrigendum in /10.3892/mmr.2016.4976. Molecular Medicine Reports, 12, 7992-8002. https://doi.org/10.3892/mmr.2015.4449
MLA
Cheng, X., Gu, J., Yuan, J., Feng, L., Jia, X."Suppression of A549 cell proliferation and metastasis by calycosin via inhibition of the PKC‑α/ERK1/2 pathway: An in vitro investigation Corrigendum in /10.3892/mmr.2016.4976". Molecular Medicine Reports 12.6 (2015): 7992-8002.
Chicago
Cheng, X., Gu, J., Yuan, J., Feng, L., Jia, X."Suppression of A549 cell proliferation and metastasis by calycosin via inhibition of the PKC‑α/ERK1/2 pathway: An in vitro investigation Corrigendum in /10.3892/mmr.2016.4976". Molecular Medicine Reports 12, no. 6 (2015): 7992-8002. https://doi.org/10.3892/mmr.2015.4449