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. Author manuscript; available in PMC: 2023 Aug 1.
Published in final edited form as: J Thorac Oncol. 2022 Jun 9;17(8):1014–1031. doi: 10.1016/j.jtho.2022.05.014

Figure 2: LSD1 abrogation induces MHC-I expression in SCLC.

Figure 2:

(A) Immunoblots of H69, H211 and H82 treated with 1μM ORY-1001 for 4, 7 and 10 days before cell lysates were collected and blotted for LSD1, B2M, di-methylated H3K4 and beta-actin protein expression. (B) Doxycycline-inducible shRNA knockdown of LSD1 (sh#1227) or non-targeting control (NTC) was performed on H82 to assess LSD1, B2M and beta-actin expression after LSD1 suppression. (C) Immunoblots of LSD1 protein level were analyzed following doxycycline-inducible shRNA knockdown in H211. (D) mRNA transcript level of KDM1A indicates shRNA knockdown of LSD1 in H211. Transcriptional activation of HLA-A, -B, -C and B2M genes were observed following (E) catalytic inhibition by ORY-1001 or (F) inducible knockdown of LSD1. Flow cytometry analysis was performed on (G) H69, (I) H211 and (L) H82 cell lines treated with either 1μM ORY-1001 for 10 days, 10ng/ml IFN-γfor 24 hours, or its combination to assess cell-surface expression of MHC-I by HLA-A,B,C antibodies. (H; K; M) Levels of increased MHC-I expression were quantitated against baseline expression from two independent experiments. Statistical significance was performed with two-way ANOVA using Geisser-Greenhouse correction; ns p>0.12; * p<0.033; ** p<0.002; and *** p<0.001.