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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 increased the number of apoptotic bodies. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 24 h. Apoptotic bodies were visualized following Hoechst 33342 staining (magnification, ×20). After treatment, apoptosis-associated morphological changes, such as chromatin condensation and apoptotic body formation were observed in HT29 cells.
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f4-mmr-12-04-5816: Ponicidin increased the number of apoptotic bodies. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 24 h. Apoptotic bodies were visualized following Hoechst 33342 staining (magnification, ×20). After treatment, apoptosis-associated morphological changes, such as chromatin condensation and apoptotic body formation were observed in HT29 cells.

Mentions: The present study also investigated whether ponicidin-induced cell growth suppression was caused by the induction of apoptosis. The HT29 cells were stained with PI and analyzed by flow cytometry. Following treatment with ponicidin, the apoptotic rate of the HT29 cells was increased to 10.2% in the 10 μg/ml group, 26.6% in the 20 μg/ml group, and 70.9% in the 50 μg/ml group, as compared with 3.9% in the untreated cells (Fig. 3). To further validate the apoptotic effects of ponicidin, the number of apoptotic bodies was determined in the treated cells (Fig. 4). Following treatment with ponicidin, a marked increase in the number of apoptotic bodies was detected in the HT29 cells. Treatment with 50 μg/ml ponicidin resulted in the most apoptotic bodies, and the highest apoptotic rate in the HT29 cells. These results were concordant with the findings regarding cell growth suppression.


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 increased the number of apoptotic bodies. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 24 h. Apoptotic bodies were visualized following Hoechst 33342 staining (magnification, ×20). After treatment, apoptosis-associated morphological changes, such as chromatin condensation and apoptotic body formation were observed in HT29 cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4-mmr-12-04-5816: Ponicidin increased the number of apoptotic bodies. HT29 human colorectal cancer cells were treated with various doses of ponicidin (10, 20 and 50 μg/ml) for 24 h. Apoptotic bodies were visualized following Hoechst 33342 staining (magnification, ×20). After treatment, apoptosis-associated morphological changes, such as chromatin condensation and apoptotic body formation were observed in HT29 cells.
Mentions: The present study also investigated whether ponicidin-induced cell growth suppression was caused by the induction of apoptosis. The HT29 cells were stained with PI and analyzed by flow cytometry. Following treatment with ponicidin, the apoptotic rate of the HT29 cells was increased to 10.2% in the 10 μg/ml group, 26.6% in the 20 μg/ml group, and 70.9% in the 50 μg/ml group, as compared with 3.9% in the untreated cells (Fig. 3). To further validate the apoptotic effects of ponicidin, the number of apoptotic bodies was determined in the treated cells (Fig. 4). Following treatment with ponicidin, a marked increase in the number of apoptotic bodies was detected in the HT29 cells. Treatment with 50 μg/ml ponicidin resulted in the most apoptotic bodies, and the highest apoptotic rate in the HT29 cells. These results were concordant with the findings regarding cell growth suppression.

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