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Positional isomerism markedly affects the growth inhibition of colon cancer cells by NOSH-aspirin: COX inhibition and modeling.

Vannini F, Chattopadhyay M, Kodela R, Rao PP, Kashfi K - Redox Biol (2015)

Bottom Line: We also analyzed the effect of these compounds on proliferation and apoptosis in HT-29 cells.The reduction of cell growth appeared to be mediated through inhibition of proliferation, and induction of apoptosis.These results suggest that the three positional isomers of NOSH-aspirin have the same biological actions, but that o-NOSH-ASA displayed the strongest anti-neoplastic potential.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Pharmacology and Neuroscience, Sophie Davis School of Biomedical Education, City University of New York Medical School, New York, NY 10031, United States.

No MeSH data available.


Related in: MedlinePlus

Positional isomers of NOSH-aspirin inhibit proliferation and increase cell death. (A) For proliferation, HT-29 cells were treated with o-NOSH-ASA, m-NOSH-ASA and p-NOSH-ASA at the concentration corresponding to their IC50s and 2×IC50s for cell growth inhibition, for 24 h, compared to control. PCNA expression was determined by flow cytometry and expressed as percentage positive cells. Results are mean±SEM of three different experiments. *P<0.05, †P<0.01 compared with untreated cells. (B) Cells were treated with the positional isomers of NOSH-ASA at their respective IC50 for cell growth inhibition and analyzed at different times for apoptosis by Annexin V- PI staining and flow cytometry. All the positional isomers of NOSH-aspirin induce apoptosis in a time-dependent manner. *P<0.05, †P<0.01 compared with untreated control cells.
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f0015: Positional isomers of NOSH-aspirin inhibit proliferation and increase cell death. (A) For proliferation, HT-29 cells were treated with o-NOSH-ASA, m-NOSH-ASA and p-NOSH-ASA at the concentration corresponding to their IC50s and 2×IC50s for cell growth inhibition, for 24 h, compared to control. PCNA expression was determined by flow cytometry and expressed as percentage positive cells. Results are mean±SEM of three different experiments. *P<0.05, †P<0.01 compared with untreated cells. (B) Cells were treated with the positional isomers of NOSH-ASA at their respective IC50 for cell growth inhibition and analyzed at different times for apoptosis by Annexin V- PI staining and flow cytometry. All the positional isomers of NOSH-aspirin induce apoptosis in a time-dependent manner. *P<0.05, †P<0.01 compared with untreated control cells.

Mentions: At 24 h, all positional isomers of NOSH-ASA reduced PCNA expression in a dose-dependent manner. Ortho, meta and para NOSH-aspirins qualitatively had similar effects on proliferation. These results are graphically represented in Fig. 3A. For o-NOSH-ASA, the proliferation decreased to 53.3±3% at its IC50 (50 nM) and 18.7±2% at 2 x IC50 (100 nM); the latter is the highest antiproliferative effect amongst the three compounds. m-NOSH-ASA decreased cell proliferation to 53.2±4% and 20.1±1%, when treated at its IC50 (250 nM) and 2×IC50 (500 nM), respectively. For p-NOSH-ASA, PCNA expression was reduced to 49.7±3% and 21.5±2% at its IC50 (500 nM) and 2×IC50 (1000 nM), respectively, compared to the untreated control.


Positional isomerism markedly affects the growth inhibition of colon cancer cells by NOSH-aspirin: COX inhibition and modeling.

Vannini F, Chattopadhyay M, Kodela R, Rao PP, Kashfi K - Redox Biol (2015)

Positional isomers of NOSH-aspirin inhibit proliferation and increase cell death. (A) For proliferation, HT-29 cells were treated with o-NOSH-ASA, m-NOSH-ASA and p-NOSH-ASA at the concentration corresponding to their IC50s and 2×IC50s for cell growth inhibition, for 24 h, compared to control. PCNA expression was determined by flow cytometry and expressed as percentage positive cells. Results are mean±SEM of three different experiments. *P<0.05, †P<0.01 compared with untreated cells. (B) Cells were treated with the positional isomers of NOSH-ASA at their respective IC50 for cell growth inhibition and analyzed at different times for apoptosis by Annexin V- PI staining and flow cytometry. All the positional isomers of NOSH-aspirin induce apoptosis in a time-dependent manner. *P<0.05, †P<0.01 compared with untreated control cells.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556775&req=5

f0015: Positional isomers of NOSH-aspirin inhibit proliferation and increase cell death. (A) For proliferation, HT-29 cells were treated with o-NOSH-ASA, m-NOSH-ASA and p-NOSH-ASA at the concentration corresponding to their IC50s and 2×IC50s for cell growth inhibition, for 24 h, compared to control. PCNA expression was determined by flow cytometry and expressed as percentage positive cells. Results are mean±SEM of three different experiments. *P<0.05, †P<0.01 compared with untreated cells. (B) Cells were treated with the positional isomers of NOSH-ASA at their respective IC50 for cell growth inhibition and analyzed at different times for apoptosis by Annexin V- PI staining and flow cytometry. All the positional isomers of NOSH-aspirin induce apoptosis in a time-dependent manner. *P<0.05, †P<0.01 compared with untreated control cells.
Mentions: At 24 h, all positional isomers of NOSH-ASA reduced PCNA expression in a dose-dependent manner. Ortho, meta and para NOSH-aspirins qualitatively had similar effects on proliferation. These results are graphically represented in Fig. 3A. For o-NOSH-ASA, the proliferation decreased to 53.3±3% at its IC50 (50 nM) and 18.7±2% at 2 x IC50 (100 nM); the latter is the highest antiproliferative effect amongst the three compounds. m-NOSH-ASA decreased cell proliferation to 53.2±4% and 20.1±1%, when treated at its IC50 (250 nM) and 2×IC50 (500 nM), respectively. For p-NOSH-ASA, PCNA expression was reduced to 49.7±3% and 21.5±2% at its IC50 (500 nM) and 2×IC50 (1000 nM), respectively, compared to the untreated control.

Bottom Line: We also analyzed the effect of these compounds on proliferation and apoptosis in HT-29 cells.The reduction of cell growth appeared to be mediated through inhibition of proliferation, and induction of apoptosis.These results suggest that the three positional isomers of NOSH-aspirin have the same biological actions, but that o-NOSH-ASA displayed the strongest anti-neoplastic potential.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Pharmacology and Neuroscience, Sophie Davis School of Biomedical Education, City University of New York Medical School, New York, NY 10031, United States.

No MeSH data available.


Related in: MedlinePlus