Experimental Research On The Regulation Of Celecoxib PI3K/Akt Signal Path To Inhibition Of Liver Cancer Cell Proliferation

ObjectiveDiscuss celecoxib inhibit the molecular mechanism of liver cancer cell linesHepG-2cell proliferation.MethodsExtracting Celecoxib in different concentration (0umol/L,6.25umol/L,12.50umol/L,25.00umol/L,50.00umol/L, and100.00umol/L) on liver cancer cellHepG-2, determined by MTT colorimetric method to detect the apoptosis of tumorcells respectively in24h,48h,72h and observation of celecoxib in vitro on humanliver cancer cells affect the cell proliferation. Using Western blot technology,observing the HepG-2cell treated with celecoxib on PI3K and p-Akt and theirdownstream products of Caspase-9, Caspase-3under the condition of differentconcentrations of protein expression changes.Results1. Longer duration of Celecoxib effect and the increase of drug dose, the role ofthe HepG-2cell proliferation inhibition enhanced obviously, doses of6.25umol/L for24h, the inhibition rate is11.50%.72h of inhibition rate is30.15%. Doses of100.00umol/L for24h, the inhibition rate are46.79%.72h the inhibition rate is74.28%(P <0.01), and have an obvious dependent on dose and time.2. Celecoxib increased with the drug concentration, PI3K, p-Akt proteinexpression levels gradually decline.After72h Celecoxib’s effect, PI3K proteins invarious concentrations relative expressions are1.62,1.43,1.09,0.79and0.59. P-Aktin the relative expression quantity of protein concentrations is respectively0.86,0.81,0.72,0.81and0.72(p <0.05). And its downstream Caspase-9in Celecoxib’s effect after72h, the relative expression of protein concentration is respectively0.71,0.98,1.21,0.98and1.21. Caspase-3in Celecoxib’s effect after72h, the relative expressionof protein concentration is respectively0.80,1.34,1.48,1.34and1.48(P <0.05).Conclusions1. Celecoxib can inhibit the HepG-2cell proliferation of liver cancer.2. Celecoxib can inhibit the PI3K/Akt signal path in the expression of PI3K,p-Akt protein raise the activity of the Caspase related-members, thus inhibiting humanliver cancer cells’ proliferation.