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. 2022 Aug 6;13(8):687. doi: 10.1038/s41419-022-05117-9

Fig. 6. BLNK triggers anoikis of ErbB2-overproducing breast cancer cells by activating p38MAPK.

Fig. 6

A, B Indicated cell lines were cultured detached from the ECM (3D) for 54 h in the absence (−) or in the presence (+) of 3 ng/ml doxycycline (doxy) and assayed for phospho-p38MAPK and p38MAPK expression by western blotting. C MCF-ErbB2-BLNK cells were cultured as in A, B for 72 h in the absence (−) or in the presence (+) of 20 μM SB203580 and counted. The number of untreated cells was designated as 100%. The data are the average of the three independent experiments plus the SD. *p-value < 0.05. D MCF10A and MCF-ErbB2 cells were cultured attached to (2D) or detached from (3D) the ECM for the indicated times and assayed as in A, B. A–G Indicated cells were cultured detached from the ECM for 6 h and assayed for ErbB2 (E), phospho-Erk1/2 (F) and IRF6 (G) levels by western blotting. α-tubulin was used as a loading control in E, G and total ERK1/2, in F. H A model of ErbB2-dependent-inhibition of breast cancer cell anoikis that emerged from our study. ErbB2-dependent ERK activation downregulates IRF6, IRF6 downregulation causes reduction in the cellular BLNK levels, while BLNK loss in turn inactivates p38MAPK and thus blocks breast cancer cell anoikis.