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. Author manuscript; available in PMC: 2021 Aug 9.
Published in final edited form as: Sci Transl Med. 2021 Feb 10;13(580):eabc6894. doi: 10.1126/scitranslmed.abc6894

Fig. 3. 17p loss renders HER2-low breast cancer cells highly vulnerable to T-Ama.

Fig. 3.

(A) Generation of 17p deletion (~20 Mb) in HS578T cells using Cas9 and two sgRNAs (sgWDR81 and sgMAP2K3). The sgRNA-targeting sites were underlined, and the protospacer adjacent motif sequence was highlighted in red. Colonies were screened using primers flanking the residual WDR81 and MAP2K3 (indicated by the arrows). Sanger sequencing results confirmed the break point junction with the deletion region indicated by the dashes. (B and C) 17pintact (B) and 17ploss (C) HS578T cells with different HER2 levels (scores 1, 2, and 3) were treated in vitro with T-Ama and T-DM1. The IC50 value is shown beside the curve. (D) Ectopic expression of POLR2A partially restored the resistance of 17ploss HS578T cells to T-Ama. IC50, half maximal inhibitory concentration; ADC, antibody-drug conjugate. The cell viability data were presented as means ± SD of three independent experiments (N = 3).