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Magnolol induces apoptosis via inhibiting the EGFR/PI3K/Akt signaling pathway in human prostate cancer cells.
J Cell Biochem. 2009 Apr 15; 106(6):1113-22.JC

Abstract

We observed that treatment of prostate cancer cells for 24 h with magnolol, a phenolic component extracted from the root and stem bark of the oriental herb Magnolia officinalis, induced apoptotic cell death in a dose- and time-dependent manner. A sustained inhibition of the major survival signal, Akt, occurred in magnolol-treated cells. Treatment of PC-3 cells with an apoptosis-inducing concentration of magnolol (60 microM) resulted in a rapid decrease in the level of phosphorylated Akt leading to inhibition of its kinase activity. Magnolol treatment (60 microM) also caused a decrease in Ser((136)) phosphorylation of Bad (a proapoptotic protein), which is a downstream target of Akt. Protein interaction assay revealed that Bcl-xL, an anti-apoptotic protein, was associated with Bad during treatment with magnolol. We also observed that during treatment with magnolol, translocation of Bax to the mitochondrial membrane occurred and the translocation was accompanied by cytochrome c release, and cleavage of procaspase-8, -9, -3, and poly(ADP-ribose) polymerase (PARP). Similar results were observed in human colon cancer HCT116Bax(+/-) cell line, but not HCT116Bax(-/-) cell line. Interestingly, at similar concentrations (60 microM), magnolol treatment did not affect the viability of normal human prostate epithelial cell (PrEC) line. We also observed that apoptotic cell death by magnolol was associated with significant inhibition of pEGFR, pPI3K, and pAkt. These results suggest that one of the mechanisms of the apoptotic activity of magnolol involves its effect on epidermal growth factor receptor (EGFR)-mediated signaling transduction pathways.

Authors+Show Affiliations

Department of Surgery and Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19229860

Citation

Lee, Dae-Hee, et al. "Magnolol Induces Apoptosis Via Inhibiting the EGFR/PI3K/Akt Signaling Pathway in Human Prostate Cancer Cells." Journal of Cellular Biochemistry, vol. 106, no. 6, 2009, pp. 1113-22.
Lee DH, Szczepanski MJ, Lee YJ. Magnolol induces apoptosis via inhibiting the EGFR/PI3K/Akt signaling pathway in human prostate cancer cells. J Cell Biochem. 2009;106(6):1113-22.
Lee, D. H., Szczepanski, M. J., & Lee, Y. J. (2009). Magnolol induces apoptosis via inhibiting the EGFR/PI3K/Akt signaling pathway in human prostate cancer cells. Journal of Cellular Biochemistry, 106(6), 1113-22. https://doi.org/10.1002/jcb.22098
Lee DH, Szczepanski MJ, Lee YJ. Magnolol Induces Apoptosis Via Inhibiting the EGFR/PI3K/Akt Signaling Pathway in Human Prostate Cancer Cells. J Cell Biochem. 2009 Apr 15;106(6):1113-22. PubMed PMID: 19229860.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Magnolol induces apoptosis via inhibiting the EGFR/PI3K/Akt signaling pathway in human prostate cancer cells. AU - Lee,Dae-Hee, AU - Szczepanski,Miroslaw-Jerzy, AU - Lee,Yong J, PY - 2009/2/21/entrez PY - 2009/2/21/pubmed PY - 2009/7/8/medline SP - 1113 EP - 22 JF - Journal of cellular biochemistry JO - J. Cell. Biochem. VL - 106 IS - 6 N2 - We observed that treatment of prostate cancer cells for 24 h with magnolol, a phenolic component extracted from the root and stem bark of the oriental herb Magnolia officinalis, induced apoptotic cell death in a dose- and time-dependent manner. A sustained inhibition of the major survival signal, Akt, occurred in magnolol-treated cells. Treatment of PC-3 cells with an apoptosis-inducing concentration of magnolol (60 microM) resulted in a rapid decrease in the level of phosphorylated Akt leading to inhibition of its kinase activity. Magnolol treatment (60 microM) also caused a decrease in Ser((136)) phosphorylation of Bad (a proapoptotic protein), which is a downstream target of Akt. Protein interaction assay revealed that Bcl-xL, an anti-apoptotic protein, was associated with Bad during treatment with magnolol. We also observed that during treatment with magnolol, translocation of Bax to the mitochondrial membrane occurred and the translocation was accompanied by cytochrome c release, and cleavage of procaspase-8, -9, -3, and poly(ADP-ribose) polymerase (PARP). Similar results were observed in human colon cancer HCT116Bax(+/-) cell line, but not HCT116Bax(-/-) cell line. Interestingly, at similar concentrations (60 microM), magnolol treatment did not affect the viability of normal human prostate epithelial cell (PrEC) line. We also observed that apoptotic cell death by magnolol was associated with significant inhibition of pEGFR, pPI3K, and pAkt. These results suggest that one of the mechanisms of the apoptotic activity of magnolol involves its effect on epidermal growth factor receptor (EGFR)-mediated signaling transduction pathways. SN - 1097-4644 UR - https://www.unboundmedicine.com/medline/citation/19229860/Magnolol_induces_apoptosis_via_inhibiting_the_EGFR/PI3K/Akt_signaling_pathway_in_human_prostate_cancer_cells_ L2 - https://doi.org/10.1002/jcb.22098 DB - PRIME DP - Unbound Medicine ER -