Limits...
Magnolol inhibits growth of gallbladder cancer cells through the p53 pathway.

Li M, Zhang F, Wang X, Wu X, Zhang B, Zhang N, Wu W, Wang Z, Weng H, Liu S, Gao G, Mu J, Shu Y, Bao R, Cao Y, Lu J, Gu J, Zhu J, Liu Y - Cancer Sci. (2015)

Bottom Line: Magnolol, the major active compound found in Magnolia officinalis has a wide range of clinical applications due to its anti-inflammation and anti-oxidation effects.The results indicated that magnolol could significantly inhibit the growth of GBC cell lines in a dose- and time-dependent manner.In conclusion, our study is the first to report that magnolol has an inhibitory effect on the growth of GBC cells and that this compound may have potential as a novel therapeutic agent for the treatment of GBC.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong, University School of Medicine, Shanghai, China.

No MeSH data available.


Related in: MedlinePlus

Magnolol-induced apoptosis and G0/G1 arrest regulated by p53. Cells were incubated for 1 h in the presence or absence of pifithrin-a (PFT-a; 20 mmol/L), and then 20 μmol/L magnolol was added for an additional 48 h. (a,b) Distribution of cells undergoing apoptosis was determined by flow cytometry. (c,d) Cell cycle distribution was determined by flow cytometry. (e) Apoptosis and G0/G1 checkpoint-related proteins were detected by Western blot. The values presented are means ± SD from three independent experiments. **P < 0.01, ***P < 0.001 versus control. CDC2, Cell division cycle 2.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4638010&req=5

fig05: Magnolol-induced apoptosis and G0/G1 arrest regulated by p53. Cells were incubated for 1 h in the presence or absence of pifithrin-a (PFT-a; 20 mmol/L), and then 20 μmol/L magnolol was added for an additional 48 h. (a,b) Distribution of cells undergoing apoptosis was determined by flow cytometry. (c,d) Cell cycle distribution was determined by flow cytometry. (e) Apoptosis and G0/G1 checkpoint-related proteins were detected by Western blot. The values presented are means ± SD from three independent experiments. **P < 0.01, ***P < 0.001 versus control. CDC2, Cell division cycle 2.

Mentions: As a transcription factor, p53 plays a central role in apoptosis and cell cycle arrest.6 Therefore, the role of p53 in magnolol-induced apoptosis and G0/G1 arrest was studied. Cells were pretreated with 20 mmol/L PFT-a, a p53 inhibitor, for 1 h before magnolol treatment for an additional 48 h. As shown in Figure5a–d, pretreatment with PFT-a prevented the magnolol-induced apoptosis and reduced G0/G1 phase cell accumulation. To investigate the possible mechanism of magnolol’s effect, we detected the protein levels of p53 and its downstream regulator p21 using Western blot analysis. The results indicated that pretreatment with PFT-a reduced the phosphorylation of p53 and the level of p21 protein (Fig.5e), suggesting that p53 and p21 activation regulate magnolol-induced apoptosis and G0/G1 phase arrest. Taken together, these data showed that magnolol initiated apoptosis and G0/G1 phase arrest through the p53 pathway.


Magnolol inhibits growth of gallbladder cancer cells through the p53 pathway.

Li M, Zhang F, Wang X, Wu X, Zhang B, Zhang N, Wu W, Wang Z, Weng H, Liu S, Gao G, Mu J, Shu Y, Bao R, Cao Y, Lu J, Gu J, Zhu J, Liu Y - Cancer Sci. (2015)

Magnolol-induced apoptosis and G0/G1 arrest regulated by p53. Cells were incubated for 1 h in the presence or absence of pifithrin-a (PFT-a; 20 mmol/L), and then 20 μmol/L magnolol was added for an additional 48 h. (a,b) Distribution of cells undergoing apoptosis was determined by flow cytometry. (c,d) Cell cycle distribution was determined by flow cytometry. (e) Apoptosis and G0/G1 checkpoint-related proteins were detected by Western blot. The values presented are means ± SD from three independent experiments. **P < 0.01, ***P < 0.001 versus control. CDC2, Cell division cycle 2.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4638010&req=5

fig05: Magnolol-induced apoptosis and G0/G1 arrest regulated by p53. Cells were incubated for 1 h in the presence or absence of pifithrin-a (PFT-a; 20 mmol/L), and then 20 μmol/L magnolol was added for an additional 48 h. (a,b) Distribution of cells undergoing apoptosis was determined by flow cytometry. (c,d) Cell cycle distribution was determined by flow cytometry. (e) Apoptosis and G0/G1 checkpoint-related proteins were detected by Western blot. The values presented are means ± SD from three independent experiments. **P < 0.01, ***P < 0.001 versus control. CDC2, Cell division cycle 2.
Mentions: As a transcription factor, p53 plays a central role in apoptosis and cell cycle arrest.6 Therefore, the role of p53 in magnolol-induced apoptosis and G0/G1 arrest was studied. Cells were pretreated with 20 mmol/L PFT-a, a p53 inhibitor, for 1 h before magnolol treatment for an additional 48 h. As shown in Figure5a–d, pretreatment with PFT-a prevented the magnolol-induced apoptosis and reduced G0/G1 phase cell accumulation. To investigate the possible mechanism of magnolol’s effect, we detected the protein levels of p53 and its downstream regulator p21 using Western blot analysis. The results indicated that pretreatment with PFT-a reduced the phosphorylation of p53 and the level of p21 protein (Fig.5e), suggesting that p53 and p21 activation regulate magnolol-induced apoptosis and G0/G1 phase arrest. Taken together, these data showed that magnolol initiated apoptosis and G0/G1 phase arrest through the p53 pathway.

Bottom Line: Magnolol, the major active compound found in Magnolia officinalis has a wide range of clinical applications due to its anti-inflammation and anti-oxidation effects.The results indicated that magnolol could significantly inhibit the growth of GBC cell lines in a dose- and time-dependent manner.In conclusion, our study is the first to report that magnolol has an inhibitory effect on the growth of GBC cells and that this compound may have potential as a novel therapeutic agent for the treatment of GBC.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong, University School of Medicine, Shanghai, China.

No MeSH data available.


Related in: MedlinePlus