Fig. 4: Knockdown of PEAK1 in MSCs abrogates their ability to promote tumorigenesis, intratumoral αSMA expression, lapatinib resistance and lapatinib-induced brain metastasis. | Oncogene

Fig. 4: Knockdown of PEAK1 in MSCs abrogates their ability to promote tumorigenesis, intratumoral αSMA expression, lapatinib resistance and lapatinib-induced brain metastasis.

From: A SNAI2-PEAK1-INHBA stromal axis drives progression and lapatinib resistance in HER2-positive breast cancer by supporting subpopulations of tumor cells positive for antiapoptotic and stress signaling markers

Fig. 4

a Western blot and relative band intensity quantification for PEAK1 and α-tubulin levels in shScramble control (shScr) and 5 different PEAK1-targeting (shP1) shRNA derivatives of C3H10T1/2 mesenchymal stem cells. Unless otherwise noted, shP1(1) construct is used throughout experiments. b Quantified primary tumor mass of CAM xenograft assay using BT474 cells only or BT474 cells xenografted together with the C3HshScr, C3HshP1(1) or C3HshP1(5) cells. c Representative images and quantification of alpha-smooth muscle actin staining of stromal tissue in CAM tumors from b. d Representative assay endpoint images for CAM xenograft experiment using the same cell combinations as in b with either vehicle control or 1 uM lapatinib treatments. e Quantified primary tumor mass of experiment in d including the treatment condition of 300 nM lapatinib. f Hematoxylin and eosin staining of CAM tumor tissue in d. g Relative metastasis of BT474 cells in the lung (left) and brain (right) of experiment in d. *, **, *** and **** indicates a p value < 0.05, 0.01, 0.001 and 0.0001, respectively, as determined by a One-Way or Two-Way ANOVA w/ multiple comparisons post-test.

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