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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Clinically relevant CHK1 inhibitors abrogate wild-type and Y537S mutant ERα expression and proliferation in luminal primary and metastatic breast cancer cells

Fig. 1

Identification of kinase inhibitor influencing ERα levels and cell proliferation in luminal primary and metastatic breast cancer cells. Robust Z scores (Z*) graphs for kinase inhibitor-treated samples (100 nM final concentration) for 48 h in Tam Res and Y537S cells. The ERα levels were detected by in-cell WB (A and B) while cell number was detected by in-cell propidium iodide (PI) staining (A’ and B’); red arrows indicate the Z* for inhibitors considered as positive hits. Red lines indicate the threshold used for analysis. Venn diagrams showing the positive hits for ERα and PI lists in Tam Res (C) and Y537S (C’) cells. (D) Venn diagram showing the combined positive hits of the inhibitors (explicated in D’ – compound names are given in brackets) in the indicated cell lines. Kaplan–Meier plots show the relapse-free survival (RFS) probability in women carrying ERα-negative (E and G) or ERα-positive (F and H) as a function of CHK1 (E and F) or CHK2 (G and H) mRNA levels. All possible cutoff values between the lower and upper quartiles are automatically computed (i.e., auto select best cutoff on the website), and the best performing threshold is used as a cutoff [27]. Details of the parameters of the curves are given in supplementary table 3. Significant differences between the RFS are given as p-value in each panel

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