Figure 3—figure supplement 3. | 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 3.

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 3.
Download figureOpen in new tabFigure 3—figure supplement 3. TGF-β signaling controls the expression of multiple HDR genes at the protein level.

(A) Western blot analysis of the expression of BRCA2, BLM and RAD50 upon vehicle or TGF-β treatment (9 hr, 1 day, 2 day, 3 day or 4 day) in H1650 cells. Phospho-Smad2 and E-cadherin are used as a marker of active TGF-β signaling and MET, respectively. α-Tubulin is used as a loading control. (B) The charts depict the quantification of the relative amounts of BRCA2, BLM and RAD50. Levels of intensity of each band were quantified using imajeJ32 software, represented as a ratio of the protein of interest to α-tubulin, and normalized to levels detected in respective TGF-β untreated (–TGF-β) samples. The data represent the mean ± SD from two independent experiments. p-value *<0.005, ***<0.001, unpaired t-test with Welch’s correction.

DOI: http://dx.doi.org/10.7554/eLife.21615.019