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1.
Asian Pacific Journal of Tropical Medicine ; (12): 87-91, 2017.
Article Dans Anglais | WPRIM | ID: wpr-820768

Résumé

OBJECTIVE@#To study whether miR-21 targets and inhibits tumor suppressor gene PTEN can promote prostate cancer cell proliferation and invasion.@*METHODS@#Prostate cancer cell lines PC-3 were cultured and divided into negative control group (NC group), miR-21 group, pcDNA3.1 group, miR-21+pcDNA3.1 group and miR-21+PTEN group that were transfected with different miR and plasmid, respectively. After 12 h and 24 h of transfection, the cell viability and invasive cell number were determined; after 24 h of transfection, Bcl-2, Survivin, MMP2, MMP9, PTEN, PI3K, and AKT expression in cells were determined.@*RESULTS@#After 12 h and 24 h of transfection, OD value and invasive cell number of miR-21 group were significantly higher than those of NC group; after 24 h of transfection, Bcl-2, Survivin, MMP2, MMP9, PI3K and AKT expression levels were significantly higher than those of NC group while PTEN expression level was significantly lower than that of NC group; after 12 h and 24 h of transfection, OD value and invasive cell number of miR-21+pcDNA3.1 group were significantly higher than those of pcDNA3.1 group, and the OD value and invasive cell number of miR-21+PTEN group were significantly lower than those of miR-21+pcDNA3.1 group; after 24 h of transfection, Bcl-2, Survivin, MMP2 and MMP9 content of miR-21+pcDNA3.1 group were significantly higher than those of pcDNA3.1 group, and Bcl-2, Survivin, MMP2 and MMP9 content of miR-21+PTEN group were significantly lower than those of miR-21+pcDNA3.1 group.@*CONCLUSIONS@#miR-21 can target and inhibit tumor suppressor gene PTEN expression to promote prostate cancer cell proliferation and invasion.

2.
Asian Pacific Journal of Tropical Medicine ; (12): 515-519, 2017.
Article Dans Anglais | WPRIM | ID: wpr-820707

Résumé

OBJECTIVE@#To study the inhibitory effect of matrine on bladder cancer cell growth and invasion in vitro through PI3K/AKT signaling pathway.@*METHODS@#Human T24 bladder cancer cell lines were cultured and treated with different doses of matrine (0.25 mg/mL, 0.5 mg/mL and 1.0 mg/mL) as well as 20 μmol/L PI3K inhibitor LY294002 for 24 h, and the cell proliferation activity, the number of invasive cells as well as the expression of p-PI3K, p-AKT, proliferation genes and invasion genes were determined.@*RESULTS@#Different doses of matrine could decrease the cell viability value, the number of invasive cells as well as the expression of p-PI3K, p-AKT, MMP2 and MMP9, and increase the expression of p16, p21 and p27 in dose-dependent manner; p16, p21 and p27 expression in cells of 20 μmol/L LY29002 group were significantly higher than those of 0 μmol/L LY29002 group while MMP2 and MMP9 expression were significantly lower than those of 0 μmol/L LY29002 group (P < 0.05).@*CONCLUSIONS@#Matrine can inhibit bladder cancer cell proliferation and invasion in vitro and regulate the expression of cell cycle-inhibiting molecules and invasion-related genes through PI3K/AKT signaling pathway.

3.
Asian Pacific Journal of Tropical Medicine ; (12): 87-91, 2017.
Article Dans Chinois | WPRIM | ID: wpr-972683

Résumé

Objective To study whether miR-21 targets and inhibits tumor suppressor gene PTEN can promote prostate cancer cell proliferation and invasion. Methods Prostate cancer cell lines PC-3 were cultured and divided into negative control group (NC group), miR-21 group, pcDNA3.1 group, miR-21+pcDNA3.1 group and miR-21+PTEN group that were transfected with different miR and plasmid, respectively. After 12 h and 24 h of transfection, the cell viability and invasive cell number were determined; after 24 h of transfection, Bcl-2, Survivin, MMP2, MMP9, PTEN, PI3K, and AKT expression in cells were determined. Results After 12 h and 24 h of transfection, OD value and invasive cell number of miR-21 group were significantly higher than those of NC group; after 24 h of transfection, Bcl-2, Survivin, MMP2, MMP9, PI3K and AKT expression levels were significantly higher than those of NC group while PTEN expression level was significantly lower than that of NC group; after 12 h and 24 h of transfection, OD value and invasive cell number of miR-21+pcDNA3.1 group were significantly higher than those of pcDNA3.1 group, and the OD value and invasive cell number of miR-21+PTEN group were significantly lower than those of miR-21+pcDNA3.1 group; after 24 h of transfection, Bcl-2, Survivin, MMP2 and MMP9 content of miR-21+pcDNA3.1 group were significantly higher than those of pcDNA3.1 group, and Bcl-2, Survivin, MMP2 and MMP9 content of miR-21+PTEN group were significantly lower than those of miR-21+pcDNA3.1 group. Conclusions miR-21 can target and inhibit tumor suppressor gene PTEN expression to promote prostate cancer cell proliferation and invasion.

4.
Asian Pacific Journal of Tropical Medicine ; (12): 515-519, 2017.
Article Dans Chinois | WPRIM | ID: wpr-972626

Résumé

Objective To study the inhibitory effect of matrine on bladder cancer cell growth and invasion in vitro through PI3K/AKT signaling pathway. Methods Human T24 bladder cancer cell lines were cultured and treated with different doses of matrine (0.25 mg/mL, 0.5 mg/mL and 1.0 mg/mL) as well as 20 μmol/L PI3K inhibitor LY294002 for 24 h, and the cell proliferation activity, the number of invasive cells as well as the expression of p-PI3K, p-AKT, proliferation genes and invasion genes were determined. Results Different doses of matrine could decrease the cell viability value, the number of invasive cells as well as the expression of p-PI3K, p-AKT, MMP2 and MMP9, and increase the expression of p16, p21 and p27 in dose-dependent manner; p16, p21 and p27 expression in cells of 20 μmol/L LY29002 group were significantly higher than those of 0 μmol/L LY29002 group while MMP2 and MMP9 expression were significantly lower than those of 0 μmol/L LY29002 group (P < 0.05). Conclusions Matrine can inhibit bladder cancer cell proliferation and invasion in vitro and regulate the expression of cell cycle-inhibiting molecules and invasion-related genes through PI3K/AKT signaling pathway.

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