Hydroxychloroquine Potentiates Apoptosis Induced by PPAR<i>α</i> Antagonist in 786-O Clear Cell Renal Cell Carcinoma Cells Associated with Inhibiting Autophagy

<div>GW6471 decreased the viability of the 786-O cells in a dose-dependent but not time-dependent manner, and GW6471 has no effect of cell viability on HK-2 cells with dose-dependent or time-dependent. (a) Cell viability of 786-O cells treated with different levels of GW6471 and WY14643 (0-75 <i>μ</i>M) for 24 h by CCK-8 assay. (b) Cell viability of 786-O cells treated with 25 <i>μ</i>M GW6471 or WY14643 for 0, 12, 24, and 48 h by CCK-8 assay. (c) Cell viability of HK-2 cells treated with different levels of GW6471 and WY14643 (0-75 <i>μ</i>M) for 24 h by CCK-8 assay. (d) Cell viability of HK-2 cells treated with 25 <i>μ</i>M GW6471 and WY14643 for 6, 12, 24, and 48 h by CCK-8 assay. 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PPAR Research

fig2

Figure 2

Figure 2: Hydroxychloroquine Potentiates Apoptosis Induced by PPAR<i>α</i> Antagonist in 786-O Clear Cell Renal Cell Carcinoma Cells Associated with Inhibiting Autophagy 

Figure 2 | Hydroxychloroquine Potentiates Apoptosis Induced by PPARα Antagonist in 786-O Clear Cell Renal Cell Carcinoma Cells Associated with Inhibiting Autophagy 