Article title: Receptor tyrosine kinase ERBB4 mediates acquired resistance to ERBB2 inhibitors in breast cancer cells
Authors: Kaleigh Canfield, Jiaqi Li, Owen M. Wilkins, Meghan M Morrison, Matthew Ung, Wendy Wells, Charlotte R Williams, Karen T Liby, Detlef Vullhorst, Andres Buonanno, Huizhong Hu, Rachel Schiff, Rebecca S Cook, and Manabu Kurokawa
Journal: Cell Cycle
Bibliometrics: Volume 14, Issue 4, Pages 648-55
DOI: 10.4161/15384101.2014.994966
The and appeared incorrectly in print and online. The correct and are provided below:
Figure 1. Pan-ERBB inhibitors cause apoptosis in BT474 cells with acquired resistance to lapatinib. (a) MTS assays reveal a panel of kinase inhibitors that attenuate proliferation of lapatinib-sensitive (left) and -resistant (right) BT474 cells (BT474 and BT474-LR, respectively). Cells were plated at a density of 1.0 × 104 per well on a 96 well plate, 18-24 hours before treatment. Cells were then treated with 1 μM of the indicated kinase inhibitors (except PD98059, U0126, and KU55933 at 10 μM). *P < 0.05 by t-test (n = 4, error bars indicate SD). (b) Lapatinib-resistant BT474 cells were treated with DMSO, lapatinib, afatinib, canertinib, dacomitinib, neratinib, or varlitinib (1 μM). Forty-eight hours later, cellular apoptosis was analyzed by Annexin V staining.
Figure 4. Genetic ablation of ERBB4 results in inhibition of the AKT pathway in lapatinib-resistant cells. siRNA knockdown of ERBB4 was performed in BT474, BT474-LR, SKBR3, and SKBR3-LR. Twenty hours later, the pan-caspase inhibitor Q-VD-OPh (20 μM) was added to prevent apoptosis. Seventy-two hours after siRNA knockdown, cell lysates were prepared and western blotting was performed to detect ERBB4, phospho-AKT (pAKT; phospho-Thr308), total AKT, phospho-ERK1/2 (pERK; phsoho-Thr202 and -Tyr204), total ERK1/2, and actin.
