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D. candidum has in vitro anticancer effects in HCT-116 cancer cells and exerts in vivo anti-metastatic effects in mice.

Zhao X, Sun P, Qian Y, Suo H - Nutr Res Pract (2014)

Bottom Line: Expression of genes commonly associated with inflammation, NF-κB, iNOS, and COX-2, was significantly downregulated by DCME.DCME also exerted an anti-metastasis effect on cancer cells as demonstrated by decreased expression of MMP genes and increased expression of TIMPs, which was confirmed by the inhibition of induced tumor metastasis in colon 26-M3.1 cells in BALB/c mice.Our results demonstrated that D. candidum had a potent in vitro anti-cancer effect, induced apoptosis, exhibited anti-inflammatory activities, and exerted in vivo anti-metastatic effects.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological and Chemical Engineering, Chongqing University of Education, China.

ABSTRACT

Background/objectives: D. candidum is a traditional Chinese food or medicine widely used in Asia. There has been little research into the anticancer effects of D. candidum, particularly the effects in colon cancer cells. The aim of this study was to investigate the anticancer effects of D. candidum in vitro and in vivo.

Materials/methods: The in vitro anti-cancer effects on HCT-116 colon cancer cells and in vivo anti-metastatic effects of DCME (Dendrobium canidum methanolic extract) were examined using the experimental methods of MTT assay, DAPI staining, flow cytometry analysis, RT-PCR, and Western blot analysis.

Results: At a concentration of 1.0 mg/mL, DCME inhibited the growth of HCT-116 cells by 84%, which was higher than at concentrations of 0.5 and 0.25 mg/mL. Chromatin condensation and formation of apoptotic bodies were observed in cancer cells cultured with DCME as well. In addition, DCME induced significant apoptosis in cancer cells by upregulation of Bax, caspase 9, and caspase 3, and downregulation of Bcl-2. Expression of genes commonly associated with inflammation, NF-κB, iNOS, and COX-2, was significantly downregulated by DCME. DCME also exerted an anti-metastasis effect on cancer cells as demonstrated by decreased expression of MMP genes and increased expression of TIMPs, which was confirmed by the inhibition of induced tumor metastasis in colon 26-M3.1 cells in BALB/c mice.

Conclusions: Our results demonstrated that D. candidum had a potent in vitro anti-cancer effect, induced apoptosis, exhibited anti-inflammatory activities, and exerted in vivo anti-metastatic effects.

No MeSH data available.


Related in: MedlinePlus

Exposure of HCT-116 human colon cancer cells to DCME induces apoptosis. (A) Appearance of apoptotic bodies in HCT-116 cells treated with different concentrations of DCME for 48 h. (B) Treatment with DCME for 48 h increased the number of apoptotic cells as measured by flow cytometry. The profile represents an increased sub-G1 population (apoptotic cells) and each point represents the mean ± SD of three independent experiments.
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Figure 1: Exposure of HCT-116 human colon cancer cells to DCME induces apoptosis. (A) Appearance of apoptotic bodies in HCT-116 cells treated with different concentrations of DCME for 48 h. (B) Treatment with DCME for 48 h increased the number of apoptotic cells as measured by flow cytometry. The profile represents an increased sub-G1 population (apoptotic cells) and each point represents the mean ± SD of three independent experiments.

Mentions: Induction of apoptosis was monitored to determine a possible mechanism underlying the inhibitory activity of DCME on HCT-116 cancer cells. The extent of chromatin condensation was analyzed by fluorescence microscopy of cells stained with the DNA-binding fluorescent dye DAPI and flow cytometric analysis. While untreated HCT-116 cells presented nuclei with homogeneous chromatin distribution, treatment with DCME induced chromatin condensation and nuclear fragmentation, suggesting the presence of apoptotic cells (Fig. 1A). Chromatin condensation and formation of apoptotic bodies, the two hallmarks of apoptosis, were observed in cells treated with 1.0 mg/mL DCME. In contrast, the level of chromatin condensation was low in cells treated with 0.25 or 0.5 mg/mL DCME. Flow cytometric analysis showed that treatment with 1.0 mg/mL D. candidum promoted apoptosis of HCT-116 cells more strongly when compared to lower concentrations of 0.25 and 0.5 mg/mL of DCME (P <0.05). This conclusion was based on the significant accumulation of cells with sub-G1 DNA content (Fig. 1B).


D. candidum has in vitro anticancer effects in HCT-116 cancer cells and exerts in vivo anti-metastatic effects in mice.

Zhao X, Sun P, Qian Y, Suo H - Nutr Res Pract (2014)

Exposure of HCT-116 human colon cancer cells to DCME induces apoptosis. (A) Appearance of apoptotic bodies in HCT-116 cells treated with different concentrations of DCME for 48 h. (B) Treatment with DCME for 48 h increased the number of apoptotic cells as measured by flow cytometry. The profile represents an increased sub-G1 population (apoptotic cells) and each point represents the mean ± SD of three independent experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4198959&req=5

Figure 1: Exposure of HCT-116 human colon cancer cells to DCME induces apoptosis. (A) Appearance of apoptotic bodies in HCT-116 cells treated with different concentrations of DCME for 48 h. (B) Treatment with DCME for 48 h increased the number of apoptotic cells as measured by flow cytometry. The profile represents an increased sub-G1 population (apoptotic cells) and each point represents the mean ± SD of three independent experiments.
Mentions: Induction of apoptosis was monitored to determine a possible mechanism underlying the inhibitory activity of DCME on HCT-116 cancer cells. The extent of chromatin condensation was analyzed by fluorescence microscopy of cells stained with the DNA-binding fluorescent dye DAPI and flow cytometric analysis. While untreated HCT-116 cells presented nuclei with homogeneous chromatin distribution, treatment with DCME induced chromatin condensation and nuclear fragmentation, suggesting the presence of apoptotic cells (Fig. 1A). Chromatin condensation and formation of apoptotic bodies, the two hallmarks of apoptosis, were observed in cells treated with 1.0 mg/mL DCME. In contrast, the level of chromatin condensation was low in cells treated with 0.25 or 0.5 mg/mL DCME. Flow cytometric analysis showed that treatment with 1.0 mg/mL D. candidum promoted apoptosis of HCT-116 cells more strongly when compared to lower concentrations of 0.25 and 0.5 mg/mL of DCME (P <0.05). This conclusion was based on the significant accumulation of cells with sub-G1 DNA content (Fig. 1B).

Bottom Line: Expression of genes commonly associated with inflammation, NF-κB, iNOS, and COX-2, was significantly downregulated by DCME.DCME also exerted an anti-metastasis effect on cancer cells as demonstrated by decreased expression of MMP genes and increased expression of TIMPs, which was confirmed by the inhibition of induced tumor metastasis in colon 26-M3.1 cells in BALB/c mice.Our results demonstrated that D. candidum had a potent in vitro anti-cancer effect, induced apoptosis, exhibited anti-inflammatory activities, and exerted in vivo anti-metastatic effects.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological and Chemical Engineering, Chongqing University of Education, China.

ABSTRACT

Background/objectives: D. candidum is a traditional Chinese food or medicine widely used in Asia. There has been little research into the anticancer effects of D. candidum, particularly the effects in colon cancer cells. The aim of this study was to investigate the anticancer effects of D. candidum in vitro and in vivo.

Materials/methods: The in vitro anti-cancer effects on HCT-116 colon cancer cells and in vivo anti-metastatic effects of DCME (Dendrobium canidum methanolic extract) were examined using the experimental methods of MTT assay, DAPI staining, flow cytometry analysis, RT-PCR, and Western blot analysis.

Results: At a concentration of 1.0 mg/mL, DCME inhibited the growth of HCT-116 cells by 84%, which was higher than at concentrations of 0.5 and 0.25 mg/mL. Chromatin condensation and formation of apoptotic bodies were observed in cancer cells cultured with DCME as well. In addition, DCME induced significant apoptosis in cancer cells by upregulation of Bax, caspase 9, and caspase 3, and downregulation of Bcl-2. Expression of genes commonly associated with inflammation, NF-κB, iNOS, and COX-2, was significantly downregulated by DCME. DCME also exerted an anti-metastasis effect on cancer cells as demonstrated by decreased expression of MMP genes and increased expression of TIMPs, which was confirmed by the inhibition of induced tumor metastasis in colon 26-M3.1 cells in BALB/c mice.

Conclusions: Our results demonstrated that D. candidum had a potent in vitro anti-cancer effect, induced apoptosis, exhibited anti-inflammatory activities, and exerted in vivo anti-metastatic effects.

No MeSH data available.


Related in: MedlinePlus