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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 suppressed cell proliferation. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 6, 12, 24 and 48 h. After treatment, cell proliferation was measured using the Cell Counting kit-8 assay (P<0.05, n=3). OD, optical density.
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f1-mmr-12-04-5816: Ponicidin suppressed cell proliferation. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 6, 12, 24 and 48 h. After treatment, cell proliferation was measured using the Cell Counting kit-8 assay (P<0.05, n=3). OD, optical density.

Mentions: To determine the suppression of cell growth by ponicidin in colorectal cancer cells, HT29 cells were treated with various doses of ponicidin for 0, 6, 12, 24 or 48 h. As shown in Fig. 1, ponicidin exerted cell growth inhibitory effects on HT29 cells in a dose-dependent manner. The growth of the HT29 cells was markedly suppressed following 48 h treatment with 50 μg/ml ponicidin, an ~4 fold reduction as compared with the untreated control cells. The suppressive effects of 10 and 20 μg/ml ponicidin were 1.5- and 2.1- fold, respectively.


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 suppressed cell proliferation. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 6, 12, 24 and 48 h. After treatment, cell proliferation was measured using the Cell Counting kit-8 assay (P<0.05, n=3). OD, optical density.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1-mmr-12-04-5816: Ponicidin suppressed cell proliferation. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 6, 12, 24 and 48 h. After treatment, cell proliferation was measured using the Cell Counting kit-8 assay (P<0.05, n=3). OD, optical density.
Mentions: To determine the suppression of cell growth by ponicidin in colorectal cancer cells, HT29 cells were treated with various doses of ponicidin for 0, 6, 12, 24 or 48 h. As shown in Fig. 1, ponicidin exerted cell growth inhibitory effects on HT29 cells in a dose-dependent manner. The growth of the HT29 cells was markedly suppressed following 48 h treatment with 50 μg/ml ponicidin, an ~4 fold reduction as compared with the untreated control cells. The suppressive effects of 10 and 20 μg/ml ponicidin were 1.5- and 2.1- fold, respectively.

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