Open Access

Regulation of the cell cycle and PI3K/Akt/mTOR signaling pathway by tanshinone I in human breast cancer cell lines

Retraction in: /10.3892/mmr.2021.12080

  • Authors:
    • Li Wang
    • Jianzhong Wu
    • Jianwei Lu
    • Rong Ma
    • Dawei Sun
    • Jinhai Tang
  • View Affiliations

  • Published online on: October 30, 2014     https://doi.org/10.3892/mmr.2014.2819
  • Pages: 931-939
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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


Abstract

Breast cancer is the second leading cause of cancer‑related mortality in females worldwide. Therefore, identifying alternative strategies to combat the disease mortality is important. The aim of the present study was to investigate the effect of tanshinone I (Tan I) on the tumorigenicity of estrogen‑responsive MCF‑7 and estrogen‑independent MDA‑MB‑453 human breast cancer cells. The cytotoxicity of Tan I was evaluated using a Cell Counting Kit‑8 assay, the apoptosis and cell cycle distribution were detected using flow cytometry and the cell morphology was observed using a fluorescence microscope. In addition, the cell cycle regulatory proteins and apoptosis‑associated proteins involved in the phosphatidylinositide 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway were detected using western blot analysis using specific protein antibodies. The MCF‑7 and MDA‑MB‑453 cells were equally sensitive to Tan I regardless of their responsiveness to estrogen. Tan I exerted similar antiproliferative activities and induction of apoptosis, resulting in S phase arrest accompanied by decreases in cyclin B and increases in cyclin E and cyclin A proteins, which may have been associated with the upregulation of cyclin‑dependent kinase inhibitors p21Cip1 and p27Kip1. In addition, Tan I was found to downregulate anti‑apoptotic and upregulate associated apoptotic components of the PI3K/Akt/mTOR signaling pathway. Notably, treatment with the PI3K inhibitor, LY294002, decreased the levels of phosphorylated (p)‑PI3K, p‑Akt and p‑mTOR. These results clearly indicated that the mechanism of action of Tan I involved, at least partially, an effect on the PI3K/Akt/mTOR signaling pathway, providing new information for anticancer drug design and development.
View Figures
View References

Related Articles

Journal Cover

February-2015
Volume 11 Issue 2

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
Wang L, Wu J, Lu J, Ma R, Sun D and Tang J: Regulation of the cell cycle and PI3K/Akt/mTOR signaling pathway by tanshinone I in human breast cancer cell lines Retraction in /10.3892/mmr.2021.12080. Mol Med Rep 11: 931-939, 2015
APA
Wang, L., Wu, J., Lu, J., Ma, R., Sun, D., & Tang, J. (2015). Regulation of the cell cycle and PI3K/Akt/mTOR signaling pathway by tanshinone I in human breast cancer cell lines Retraction in /10.3892/mmr.2021.12080. Molecular Medicine Reports, 11, 931-939. https://doi.org/10.3892/mmr.2014.2819
MLA
Wang, L., Wu, J., Lu, J., Ma, R., Sun, D., Tang, J."Regulation of the cell cycle and PI3K/Akt/mTOR signaling pathway by tanshinone I in human breast cancer cell lines Retraction in /10.3892/mmr.2021.12080". Molecular Medicine Reports 11.2 (2015): 931-939.
Chicago
Wang, L., Wu, J., Lu, J., Ma, R., Sun, D., Tang, J."Regulation of the cell cycle and PI3K/Akt/mTOR signaling pathway by tanshinone I in human breast cancer cell lines Retraction in /10.3892/mmr.2021.12080". Molecular Medicine Reports 11, no. 2 (2015): 931-939. https://doi.org/10.3892/mmr.2014.2819