| 1. |
|
|
| 2. |
|
|
| 3. |
- Liu, Jian-Jun, et al.
(author)
-
LY294002 Enhances Boswellic Acid-induced Apoptosis in Colon Cancer Cells
- 2009
-
In: Anticancer research. - 1791-7530. ; 29:8, s. 2987-2991
-
Journal article (peer-reviewed)abstract
- Background: Boswellic acids, a type of pentacyclic triterpenoids, have been shown to induce apoptosis in colon cancer cells. The phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) pathway is crucial for cell proliferation and survival. Whether the apoptotic effects of boswellic acid could be affected by inhibition of PI3K/Akt pathway was examined. Materials and Methods: Colon cancer HT29 cells were treated with 3-acetyl-11-keto-beta boswellic acid AKBA in the absence and presence of LY294002 or Wortmanin, inhibitors of PI3K. Apoptosis was determined by flow cytometry and caspase assay. The activation of Akt was examined by Western blot. Results: AKBA at 30 mu M only slightly induced apoptosis. Preincubation of the cells with LY294002 or wortmannin significantly enhanced the AKBA-induced apoptosis up to 20-fold. Further study showed that at the doses used, AKBA induced phosphorylation of Akt at both Ser473 and Thr308 positions, indicating an activation of the PI3K/Akt pathway. Conclusion: AKBA may activate the PI3K/Akt pathway and inhibition of the P13K pathway significantly enhances AKBA-induced apoptosis.
|
|
| 4. |
- Liu, Jian-Jun, et al.
(author)
-
Sulindac induces apoptosis, inhibits proliferation and activates caspase-3 in Hep G2 cells
- 2002
-
In: Anticancer research. - 1791-7530. ; 22:1A, s. 263-266
-
Journal article (peer-reviewed)abstract
- Background: It has recently been reported that sulindac has an apoptotic effect on KYN-2 cells, an undifferentiated hepatoma cell line. The present work investigates whether sulindac also has an apoptotic effect on well-differentiated hepatoma cells and what its potential mechanism might be. Materials and Methods: Hep G2 cells were treated with sulindac at different concentrations. Apoptosis rate, cell proliferation and 3H-thymidine incorporation were measured. The activities of caspase-3, acid and neutral sphingomyelinase and the changes of sphingomyelin content were also assayed. Results: Sulindac dose-dependently induced apoptosis in Hep G2 cells; both sulindac sulfone and sulfide had similar effects. The apoptosis was accompanied by an increase 3 of caspase-3 activity and a decrease of cell proliferation and H-3-thymidine incorporation. No significant change could be observed for the activity of sphingomyelinase and sphingomyelin content. Conclusion: Sulindac induces apoptosis and inhibits proliferation in Hep G2 cells. The effect may, be mediated by, a pathway related to caspase-3 activation but independent of sphingomyelin metabolism.
|
|
| 5. |
- Villagomez, Rodrigo, et al.
(author)
-
Multiple Anticancer Effects of Damsin and Coronopilin Isolated from Ambrosia arborescens on Cell Cultures.
- 2013
-
In: Anticancer research. - 1791-7530. ; 33:9, s. 3799-3805
-
Journal article (peer-reviewed)abstract
- Terpenoids in plants are important sources for drug discovery. In this study, we extracted damsin and coronopilin, two sesquiterpene lactones, from Ambrosia arborescens and examined their anticancer effects on cell cultures. Damsin and coronopilin inhibited cell proliferation, DNA biosynthesis and formation of cytoplasmic DNA histone complexes in Caco-2 cells, with damsin being more potent than coronopilin. Further studies using the luciferase reporter system showed that damsin and coronopilin also inhibited expressions of nuclear factor-κB (NF-κB) and signal transducer and activator of transcription-3 (STAT3), indicating that these sesquiterpenes can interfere with NF-κB and STAT3 pathways. Finally, we examined the effects of two synthetic dibrominated derivatives of damsin, 11α,13-dibromodamsin and 11β,13-dibromodamsin. While bromination appeared to weaken the antiproliferative effects of damsin, the β epimer had strong inhibitory effects on STAT3 activation. In conclusion, the sesquiterpene lactones damsin and coronopilin have inhibitory effects on cell proliferation, DNA biosynthesis and NF-κB and STAT3 pathways, thus being potentially important for discovery of drugs against cancer.
|
|
| 6. |
- Zhang, Ping, et al.
(author)
-
Dietary Sphingomyelin Inhibits Colonic Tumorigenesis with an Up-regulation of Alkaline Sphingomyelinase Expression in ICR Mice
- 2008
-
In: Anticancer research. - 1791-7530. ; 28:6A, s. 3631-3635
-
Journal article (peer-reviewed)abstract
- Background: Sphingomyelin (SM) hydrolysis generates biologically active products regulating cell growth, differentiation and apoptosis. Dietary SM has been found to inhibit colonic tumorigenesis. Alkaline sphingomyelinase (alk-SMase) is the key enzyme responsible for sphingomyelin digestion in the gut. Whether or not dietary sphingomyelin affects alk-SMase expression was examined in a colon cancer animal model. Materials and Methods: Imprinting control region (ICR) mice were injected with 1,2-dimethylhydrazine (DMH) and then fed a diet with or without SM (0.5 g/kg in diet) for 22 weeks. The colonic tumorigenesis and alk-SMase activity were determined and alk-SMase expression was examined by Western blot and PCR. Results: Dietary SM inhibited the tumorigenesis and increased the alk-SMase activity in the colon by 65%. The increased activity was associated with increased enzyme protein and mRNA expression. No changes of acid and neutral sphingomyelinase activities were found. Conclusion: Long-term supplementation with dietary sphingomyelin up-regulates colonic alk-SMase expression, which may contribute to the inhibitory effects of sphingomyelin against colonic carcinogenesis.
|
|
