Open Access

Parthenolide facilitates apoptosis and reverses drug-resistance of human gastric carcinoma cells by inhibiting the STAT3 signaling pathway

  • Authors:
    • Hua Li
    • Hang Lu
    • Meng Lv
    • Qingsheng Wang
    • Yuping Sun
  • View Affiliations

  • Published online on: January 8, 2018     https://doi.org/10.3892/ol.2018.7739
  • Pages: 3572-3579
  • Copyright: © Li 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

In the present study, SGC‑7901/DDP cells were treated with different concentrations of parthenolide (PN) (2.5‑15 µmol/l), cisplatin (DDP) (1.25‑15 µg/ml) and PN+DDP. The proliferation inhibition rates were measured using an MTT assay, and the synergies of PN and DDP were analyzed. The effect of PN and DDP on SGC‑7901/DDP cell proliferation demonstrated a time‑ and concentration‑dependent association, and a synergy between PN and DDP was identified. DAPI staining and flow cytometry results indicated that 15 µmol/l PN significantly induced SGC‑7901/DDP apoptosis and G1 phase arrest compared with the untreated control group. Western blotting analysis results indicated that among the apoptosis‑associated proteins, there were dose‑dependent increases in the protein expression of apoptosis regulator BAX, cellular tumor antigen p53, cleaved caspase‑3 and cleaved capase‑9, and decreases in apoptosis regulator Bcl‑2 and Bcl‑xL protein expression levels. Among the cell cycle‑associated proteins, cyclin D1 expression was significantly decreased, cyclin‑dependent kinase inhibitor 1 expression was significantly increased, and signal transducer and activator of transcription 3 (STAT3) activation was inhibited. Scratch and Transwell assay results revealed that PN significantly inhibited SGC‑7901/DDP cell migration, and invasion. The present study demonstrated that PN induces SGC‑7901/DDP apoptosis, inhibits SGC‑7901/DDP proliferation, migration and invasion, and enhances the drug sensitivity of the cells to DDP. The underlying mechanisms may be associated with inhibition of the STAT3 signaling pathway and regulation of the downstream apoptotic protein and cyclin expression levels.
View Figures
View References

Related Articles

Journal Cover

March-2018
Volume 15 Issue 3

Print ISSN: 1792-1074
Online ISSN:1792-1082

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Li H, Lu H, Lv M, Wang Q and Sun Y: Parthenolide facilitates apoptosis and reverses drug-resistance of human gastric carcinoma cells by inhibiting the STAT3 signaling pathway. Oncol Lett 15: 3572-3579, 2018
APA
Li, H., Lu, H., Lv, M., Wang, Q., & Sun, Y. (2018). Parthenolide facilitates apoptosis and reverses drug-resistance of human gastric carcinoma cells by inhibiting the STAT3 signaling pathway. Oncology Letters, 15, 3572-3579. https://doi.org/10.3892/ol.2018.7739
MLA
Li, H., Lu, H., Lv, M., Wang, Q., Sun, Y."Parthenolide facilitates apoptosis and reverses drug-resistance of human gastric carcinoma cells by inhibiting the STAT3 signaling pathway". Oncology Letters 15.3 (2018): 3572-3579.
Chicago
Li, H., Lu, H., Lv, M., Wang, Q., Sun, Y."Parthenolide facilitates apoptosis and reverses drug-resistance of human gastric carcinoma cells by inhibiting the STAT3 signaling pathway". Oncology Letters 15, no. 3 (2018): 3572-3579. https://doi.org/10.3892/ol.2018.7739