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Ponicidin suppresses HT29 cell growth via the induction of G1 cell cycle arrest and apoptosis.

Du J, Chen C, Sun Y, Zheng L, Wang W - Mol Med Rep (2015)

Bottom Line: Western blot analysis was used to measure the expression levels of apoptosis‑associated proteins following treatment with ponicidin.The AKT and MEK signaling pathways were also suppressed by ponicidin; however, the p38 signaling pathway was significantly activated.These results suggest that ponicidin exerts significant antitumor effects via the induction of cell cycle arrest and apoptosis in colorectal cells.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Port Hospital of Tianjin, Tianjin 300456, P.R. China.

ABSTRACT
Ponicidin is a diterpenoid extracted from the Chinese herb Isodon adenolomus, which has been reported as a therapeutic cytotoxic drug that may be used to treat various types of human cancer. The present study aimed to determine the antitumor effects of ponicidin, and to investigate its underlying mechanisms in colorectal cancer. The HT29 colorectal cancer cell line was used to detect the cytotoxicity of various doses of ponicidin. Cell proliferation was measured using a Cell Counting kit‑8 assay. Cell cycle and apoptosis analyses were performed using flow cytometry and fluorescent microscopy. Western blot analysis was used to measure the expression levels of apoptosis‑associated proteins following treatment with ponicidin. Treatment with ponicidin significantly suppressed HT29 cell growth by inducing G1 cell cycle arrest and apoptosis. The AKT and MEK signaling pathways were also suppressed by ponicidin; however, the p38 signaling pathway was significantly activated. The expression levels of caspase 3 and Bax protein were markedly upregulated following treatment with ponicidin. These results suggest that ponicidin exerts significant antitumor effects via the induction of cell cycle arrest and apoptosis in colorectal cells. In conclusion, ponicidin acted as an inducer of apoptosis, and may be used as a therapeutic cytotoxic drug to treat human cancer, including colorectal cancer.

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Related in: MedlinePlus

Ponicidin induced cell cycle arrest. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 or 50 μg/ml) for 24 h. Cell cycle analysis was performed by fluorescence-activated cell sorting (FACS) in HT29 cells. DNA was stained with propidium iodide. Relative phase group was calculated by FACS (P<0.05, n=3).
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f2-mmr-12-04-5816: Ponicidin induced cell cycle arrest. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 or 50 μg/ml) for 24 h. Cell cycle analysis was performed by fluorescence-activated cell sorting (FACS) in HT29 cells. DNA was stained with propidium iodide. Relative phase group was calculated by FACS (P<0.05, n=3).

Mentions: In order to investigate the underlying mechanism of ponicidin-induced cell growth suppression, cell cycle analysis was performed on the HT29 cells treated with various doses of ponicidin. Treatment with ponicidin suppressed DNA synthesis and cell proliferation, as evidenced by a reduced percentage of S-phase cells (19.02% in the 10 μg/ml group, 11.23% in the 20 μg/ml group, and 7.17% in the 50 μg/ml group, as compared with 14.05% in the control group). G1 cell cycle arrest was markedly increased following treatment with ponicidin (53.89% in the 10 μg/ml group, 60.71% in the 20 μg/ml group, and 66.33% in the 50 μg/ml group, as compared with 51.02% in the control group) (Fig. 2).


Ponicidin suppresses HT29 cell growth via the induction of G1 cell cycle arrest and apoptosis.

Du J, Chen C, Sun Y, Zheng L, Wang W - Mol Med Rep (2015)

Ponicidin induced cell cycle arrest. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 or 50 μg/ml) for 24 h. Cell cycle analysis was performed by fluorescence-activated cell sorting (FACS) in HT29 cells. DNA was stained with propidium iodide. Relative phase group was calculated by FACS (P<0.05, n=3).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581821&req=5

f2-mmr-12-04-5816: Ponicidin induced cell cycle arrest. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 or 50 μg/ml) for 24 h. Cell cycle analysis was performed by fluorescence-activated cell sorting (FACS) in HT29 cells. DNA was stained with propidium iodide. Relative phase group was calculated by FACS (P<0.05, n=3).
Mentions: In order to investigate the underlying mechanism of ponicidin-induced cell growth suppression, cell cycle analysis was performed on the HT29 cells treated with various doses of ponicidin. Treatment with ponicidin suppressed DNA synthesis and cell proliferation, as evidenced by a reduced percentage of S-phase cells (19.02% in the 10 μg/ml group, 11.23% in the 20 μg/ml group, and 7.17% in the 50 μg/ml group, as compared with 14.05% in the control group). G1 cell cycle arrest was markedly increased following treatment with ponicidin (53.89% in the 10 μg/ml group, 60.71% in the 20 μg/ml group, and 66.33% in the 50 μg/ml group, as compared with 51.02% in the control group) (Fig. 2).

Bottom Line: Western blot analysis was used to measure the expression levels of apoptosis‑associated proteins following treatment with ponicidin.The AKT and MEK signaling pathways were also suppressed by ponicidin; however, the p38 signaling pathway was significantly activated.These results suggest that ponicidin exerts significant antitumor effects via the induction of cell cycle arrest and apoptosis in colorectal cells.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Port Hospital of Tianjin, Tianjin 300456, P.R. China.

ABSTRACT
Ponicidin is a diterpenoid extracted from the Chinese herb Isodon adenolomus, which has been reported as a therapeutic cytotoxic drug that may be used to treat various types of human cancer. The present study aimed to determine the antitumor effects of ponicidin, and to investigate its underlying mechanisms in colorectal cancer. The HT29 colorectal cancer cell line was used to detect the cytotoxicity of various doses of ponicidin. Cell proliferation was measured using a Cell Counting kit‑8 assay. Cell cycle and apoptosis analyses were performed using flow cytometry and fluorescent microscopy. Western blot analysis was used to measure the expression levels of apoptosis‑associated proteins following treatment with ponicidin. Treatment with ponicidin significantly suppressed HT29 cell growth by inducing G1 cell cycle arrest and apoptosis. The AKT and MEK signaling pathways were also suppressed by ponicidin; however, the p38 signaling pathway was significantly activated. The expression levels of caspase 3 and Bax protein were markedly upregulated following treatment with ponicidin. These results suggest that ponicidin exerts significant antitumor effects via the induction of cell cycle arrest and apoptosis in colorectal cells. In conclusion, ponicidin acted as an inducer of apoptosis, and may be used as a therapeutic cytotoxic drug to treat human cancer, including colorectal cancer.

Show MeSH
Related in: MedlinePlus