Nuclear PKM2 contributes to gefitinib resistance via upregulation of STAT3 activation in colorectal cancer

• Published in: Scientific reports Vol. 5; no. 1; p. 16082
• Main Authors: Li, Qiong, Zhang, Daoxiang, Chen, Xiaoying, He, Lei, Li, Tianming, Xu, Xiaoping, Li, Min
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 06.11.2015; Nature Publishing Group
• Subjects: 13/109; 13/2; 13/31; 13/44; 13/89; 14/19; 14/63; 64/60; 692/308/1892; 692/4028/67/1059/602; 82/29; 82/80; 96/1; Antineoplastic Agents - pharmacology; Brain tumors; Carrier Proteins - genetics; Cell Line; Cell Line, Tumor; Cell Nucleus - drug effects; Cell Nucleus - genetics; Clinical trials; Colorectal cancer; Colorectal carcinoma; Colorectal Neoplasms - drug therapy; Colorectal Neoplasms - genetics; Drug Resistance, Neoplasm - genetics; Enzyme inhibitors; Epidermal growth factor; Epidermal growth factor receptors; ErbB Receptors - genetics; Gefitinib; Glioma; HCT116 Cells; HEK293 Cells; HT29 Cells; Humanities and Social Sciences; Humans; Inhibitor drugs; Lung cancer; Membrane Proteins - genetics; multidisciplinary; Protein Kinase Inhibitors - pharmacology; Protein-tyrosine kinase; Pyruvate kinase; Pyruvic acid; Quinazolines - pharmacology; Science; siRNA; Stat3 protein; STAT3 Transcription Factor - genetics; Targeted cancer therapy; Thyroid Hormone-Binding Proteins; Thyroid Hormones - genetics; Transcription; Transcriptional Activation - genetics; Up-Regulation - genetics

Gefitinib (Iressa, ZD-1839), a small molecule tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) pathway, is currently under investigation in clinical trials for the treatment of colorectal cancer (CRC). However, as known, some patients develop resistance to TKIs and the...