10.6084/m9.figshare.8426330.v1 Ronan McLaughlin Ronan McLaughlin Jichao He Jichao He Vera Noord Vera Noord Jevin Redel Jevin Redel John Foekens John Foekens John Martens John Martens Marcel Smid Marcel Smid Yinghui Zhang Yinghui Zhang Bob Water Bob Water Additional file 3: of A kinase inhibitor screen identifies a dual cdc7/CDK9 inhibitor to sensitise triple-negative breast cancer to EGFR-targeted therapy Springer Nature 2019 CDK9/Cdc7 inhibition EGFR-targeted therapy Drug resistance Triple-negative breast cancer 2019-07-01 05:00:00 Journal contribution https://springernature.figshare.com/articles/journal_contribution/Additional_file_3_of_A_kinase_inhibitor_screen_identifies_a_dual_cdc7_CDK9_inhibitor_to_sensitise_triple-negative_breast_cancer_to_EGFR-targeted_therapy/8426330 Figure S1. Resistance of TNBC cells to EGFR-TKIs. a. Effect of lapatinib on induction of apoptosis in selected lapatinib-resistant and lapatinib-sensitive TNBC cell lines. Hs578T, BT549, SKBR7 and HCC1806 cells were treated with lapatinib (3.16 μM) as indicated, for 24 h, 48 h or 72 h, respectively, stained with Annexin-V and Hoechst, followed by imaging and image quantification. Relative cell death was quantified by normalising the intensity of Annexin-V signal to that of DMSO control. One-way ANOVA **** P ≤ 0.0001, *** P ≤ 0.001, ** P ≤ 0.01, * P ≤ 0.05. b. Impact of silencing EGFR and downstream components of EGFR signalling pathway on the proliferation of Hs578T cells. Hs578T cells were transfected with siRNAs targeting EGFR, ERK2 and FRAP1 as well as positive (siKIF11) and negative controls (siGAPDH and siKinase Pool) as described and grown for 4 days. Proliferation was then assessed using sulphorhodamine B assay. Results were normalised to Kinase Pool using the % control method as described in materials and methods. (PDF 191 kb)