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. 2019 Aug 28;39(1):50–63. doi: 10.1038/s41388-019-0953-9

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© The Author(s) 2019, corrected publication 2024

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Fig. 4 — CDK7/RNA Pol II activity is regulated by receptor tyrosine kinases and their downstream pathways. a Expression and phosphorylation of CDK7 and RNA Pol II in HMEC cells stably overexpressing HER2 inhibitor-resistant RTKs. b Immunoblot analysis of ERK and AKT signaling pathways in HMECs with ectopic expression of wild-type and mutant SHP2. c Immunoblot analysis of CDK7 and RNA Pol II in HMECs with ectopic expression of mutant PI3KCA and wild-type AKT1. d Proposed mechanism of CKD7 transcriptional regulation by RTKs. e Overlap of genes that were upregulated by PI3K and SHP2 in HMECs. Genes inhibited by THZ1 in HER2+ BCs were circled in green. f Q RT-PCR analysis mRNA expression of MYC and TWIST in both HMEC-PIK3CA^H1047R and HEMC-SHP2^E76A HER2 cells, compared the vector control cell HMEC-pBABE, Data represent mean ± SD (n = 3). **p < 0.01 (Student’s t test). g, h, i Cells were treated with lapatinib or THZ1 for 24 h and the mRNA levels were determined using Q RT-PCR. Data represent mean ± SD (n = 3). *p < 0.05; **p < 0.01; ***p < 0.001 (Student’s t test)