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)