Corrections:

Yu-Chin Lin^1,2,3, Meng-Hsuan Wu^1,*, Tzu-Tang Wei^1,*, Yun-Chieh Lin^1,*, Wen-Chih Huang⁴, Liang-Yu Huang¹, Yi-Ting Lin¹, and Ching-Chow Chen¹

¹ Graduate Institute of Pharmacology, National Taiwan University College of Medicine;
² Department of Oncology, National Taiwan University Hospital;
³ Department of Internal Medicine and
⁴ Department of Pathology, Far-Eastern Memorial Hospital;
^* Equal contribution to work

Published: October 01, 2019

This article has been corrected: The proper images for Figure 3 and Figure 4 are shown below. The authors declare that these corrections do not change the results or conclusions of this paper.

Original article: Oncotarget. 2019; 10:3577–3578. DOI: https://doi.org/10.18632/oncotarget.1628.

Figure 3: AMPK activation mediated dasatinib-induced ER stress and EGFR degradation. (A) The effect of dasatinib on AMPK activation. Cells were treated with dasatinib (1uM) for indicated intervals. The expression of p-AMPK and AMPK was evaluated. (B) The effect of AMPK knockdown on dasatinib-induced EGFR degradation and ER stress. Cells were treated with control or AMPK siRNA and then with dasatinib for 24 hours. (C) The effect of AMPK activation on dasatinib-induced EGFR degradation. Cells were treated with dasatinib with or without AICAR (10uM) for 24 hours. The expression of EGFR p-eIF2α, and AMPK was evaluated. (D) The correlation between p-AMPK and EGFR expression. Left, the expression of EGFR, p-AMPK, and AMPK in HNSCC cells. Right, the correlation of p-AMPK and EGFR expression in resected human specimens. Pearson’s correlation coefficient=0.659; *, p<0.01.

Figure 4: Dasatinib induced cellular ATP decrease and PDK4 up-regulation. (A,B) The effect of 6-hr or 18-hr dasatinib (1uM) on cellular ATP (A) and glucose (B) levels. *, p<0.05. (C) The expression of PDK4 and p-Erk in HNSCC cells treated with dasatinib (1uM) for indicated intervals.