Fig. 7: Cholesterol metabolic alteration renders LILRB1-KD MM cells sensitivity to ferroptosis by upregulating SQLE and downregulating squalene.

a, b Western blot showing the expression of LDLR, SQLE, GAPDH in CTR-KD or LILRB1-KD MM cells treated with or without cholesterol (a) or LDL (b). The independent experiments were repeated three times and the representative images are shown. c Schematic diagram showing the mechanism underlying LILRB1’s role in maintaining cholesterol balance and inhibitors in cholesterol synthesis pathway. d–f Cell death of CTR-KD or LILRB1-KD MM cells treated with 10 h RSL3 (400 nM) and/or different inhibitors in cholesterol synthesis pathway [simvastatin (10 µM) (d), terbinafine (20 µM) (e), or NB598 (5 µM) (f)]. g CTR-KD or LILRB1-KD MM cells were counted and harvested, followed by detection of squalene levels in cells by HPLC-MS. Data are representative of at least three independent experiments and are presented as mean ± SD. (d–f) -ARP1, n = 6; (d–f)-MOLP-8, n = 5; g, n = 3; n, independent experimental repeats; For (d–f), statistical significance was determined by two-tailed Student t-test; For (g), statistical significance was determined by one-tailed Student t-test. Source data are provided as a Source Data file.