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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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Ponicidin regulated apoptosis-associated protein expression. (A) HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 24 h. The expression levels of cell apoptosis-associated proteins were measured by western blotting. (B) Relative protein expression levels were quantified by Quantity One software.
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f5-mmr-12-04-5816: Ponicidin regulated apoptosis-associated protein expression. (A) HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 24 h. The expression levels of cell apoptosis-associated proteins were measured by western blotting. (B) Relative protein expression levels were quantified by Quantity One software.

Mentions: In order to investigate the molecular mechanism underlying ponicidin-induced apoptosis in HT29 cells, apoptosis-associated protein expression was measured by western blot analysis. As shown in Fig. 5, the expression levels of p-p38 were markedly increased following treatment with ponicidin (4.4-fold increase in the 10 μg/ml group, 4.4-fold increase in the 20 μg/ml group and 8.3-fold increase in the 50 μg/ml group), whereas total p38 protein expression levels remained unchanged. Similarly, apoptotic markers, caspase 3 and Bax were markedly upregulated in the treated cells; however, p-AKT and p-ERK were downregulated in the treated cells. These results indicate that proliferation signaling pathways were suppressed following treatment with ponicidin (Fig. 5).


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 regulated apoptosis-associated protein expression. (A) HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 24 h. The expression levels of cell apoptosis-associated proteins were measured by western blotting. (B) Relative protein expression levels were quantified by Quantity One software.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f5-mmr-12-04-5816: Ponicidin regulated apoptosis-associated protein expression. (A) HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 24 h. The expression levels of cell apoptosis-associated proteins were measured by western blotting. (B) Relative protein expression levels were quantified by Quantity One software.
Mentions: In order to investigate the molecular mechanism underlying ponicidin-induced apoptosis in HT29 cells, apoptosis-associated protein expression was measured by western blot analysis. As shown in Fig. 5, the expression levels of p-p38 were markedly increased following treatment with ponicidin (4.4-fold increase in the 10 μg/ml group, 4.4-fold increase in the 20 μg/ml group and 8.3-fold increase in the 50 μg/ml group), whereas total p38 protein expression levels remained unchanged. Similarly, apoptotic markers, caspase 3 and Bax were markedly upregulated in the treated cells; however, p-AKT and p-ERK were downregulated in the treated cells. These results indicate that proliferation signaling pathways were suppressed following treatment with ponicidin (Fig. 5).

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