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THE MECHANISM OF PPARN3 MEDIATED DOWN REGULATION OF SODIUM HYDROGEN EXCHANGER 1 (NHE1) GENE EPXRESSION AND ITS INHIBITION BY ESTROGEN RECEPTOR n1 3

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Figure 13: Effects of PPARγ ligands on breast cancer cell morphology and cell viability. (A) MCF-7 (3 X10 cells/6-well dishes) and MDA-MB-231 (2 X 105 cells/6-well dishes) cells were treated with 15d-PGJ2, for 24h, and pictures were taken to show 110 the morphology of the cells. (B) MCF-7 (3 X105 cells/6-well dishes) cells were treated with ciglitazone for 24h before pictures were taken to show the morphology of the cells. (C) MCF-7 (1.5X105 cells/12-well dishes) cells were treated with 15d-PGJ2, for 24h, before crystal violet assay was used to determine cell viability as described in Materials and Methods. Results denote means +/-SD computed from two experiments done in duplicate. *, p . 15 d-PGJ 2 , while 15 d-PGJ 2 resulted in the maximal reduction in the number of colonies formed by MDA-MB-2 31 cells expressing the highest level of PPARγ receptor. 11 3 Figure 14 : PPARγ agonists. 11 0 Figure 13 : Effects of PPARγ ligands on breast cancer cell morphology and cell viability. (A) MCF-7 (3 X10 5 cells/6-well dishes) and MDA-MB-2 31 (2 X 10 5 cells/6-well. reproductive inhibition triggered by PPARγ ligands. To further accertain that the colonogenic inhibition by 15 d-PGJ 2 is common in other PPARγ expressing breast cancer cell lines, MDA-MB-2 31 and T47D

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