Figure 3—figure supplement 4. | TGF-β reduces DNA ds-break repair mechanisms to heighten genetic diversity and adaptability of CD44+/CD24− cancer cells

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TGF-β reduces DNA ds-break repair mechanisms to heighten genetic diversity and adaptability of CD44+/CD24− cancer cells

Figure 3—figure supplement 4.

Affiliation details

Cold Spring Harbor Laboratory, United States; Stony Brook University, United States; Huntington Hospital, Northwell Health, United States; University of Southern California, United States; Cancer Research UK – Cambridge Institute, University of Cambridge, United Kingdom
Figure 3—figure supplement 4.
Download figureOpen in new tabFigure 3—figure supplement 4. Inhibition of TGF-β signaling in the CD44+/CD24− H1650-M3 cells results in an increased expression of HDR genes.

(A) TGF-β receptor 1 (TGFBR1) kinase activity was blocked by treatment with 1 uM LY364947 (Selleckchem) for 48–72 hr. Expression of TGF-β signature genes were used as a control for the efficacy of LY364947 treatment. mRNA expression was quantified through SYBR-green-based RT-qPCR. Each bar represents the mean ± SD of three replicates from two independent experiments (p-value *<0.05, **<0.005 paired t-test). (B) Western blot analysis of H1650 and H1650-M3 cells treated with LY364947 (1 uM) shows that the inhibitor specifically inhibits TGF-β signaling, as phosphorylation of Smad2 and Smad3 are repressed after 48 hr of treatment.

DOI: http://dx.doi.org/10.7554/eLife.21615.020