Supplementary Figure 3: ALOX12 is critical for p53-mediated ferroptosis in H1299 Tet-on p533KR cells. | Nature Cell Biology

Supplementary Figure 3: ALOX12 is critical for p53-mediated ferroptosis in H1299 Tet-on p533KR cells.

From: ALOX12 is required for p53-mediated tumour suppression through a distinct ferroptosis pathway

Supplementary Figure 3

(a) Western blot analysis of H1299 Tet-on p533KR control or ALOX12 crispr clones #3 and #4. The experiments were repeated twice, independently, with similar results. (b) H1299 Tet-on p533KR control or ALOX12 crispr clones #4, from a, were pre-incubated with doxycycline (0.5ug/ml) for 12h, then treated with doxycycline (0.5 ug/ml), and TBH (60uM) as indicated for 8h. Quantification of cell death is shown. Error bars are mean ± s.d., n = 3 independent experiments. (c) H1299 Tet-on p533KR control or ALOX12 crispr clones #4, from a, were pre-incubated with doxycycline (0.5ug/ml) for 12h, then treated with doxycycline (0.5 ug/ml), and TBH (60uM) for indicated times. Quantification of cell death is shown. Error bars are mean ± s.d., n = 3 independent experiments. (d)Tumor weight (mg) (each group has n = 3 independent samples) was determined shown in Fig. 2f. Error bars are mean ± s.d. (e) Western blot analysis of xenograft tumors from H1299 Tet-on p533KR control and ALOX12 crispr shown in Fig. 2f. The experiments were repeated twice, independently, with similar results. All P values were calculated using two-tailed unpaired Student’s t-test. Scanned images of unprocessed blots are shown in Supplementary Fig. 9. Raw data are provided in Supplementary Table 1.

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