This article has been regretfully retracted at the request of the authors due to mistakes which occurred during the figure preparation. Although the authors published a corrigendum about these mistakes (Cancer Lett. 2016 Aug 1. pii: S0304-3835 (16) 30443-8), they now feel that it is more appropriate to retract the paper to keep their research at a high standard. All authors have agreed to this decision and apologize for any inconvenience caused by retraction of this article.

se ut uy Ka y Sch tion of M ing the past few years, the identiï¬ cation of activating mutations in survival compared with standard platinum-based chemotherapy [5–7]. Furthermore, the recent identiï¬ cation of anaplastic lym-phoma kinase (ALK) gene rearrangements in NSCLC represents an-nase and ALK inhibitors-based therapies is common [13–15], high-peutic targets for factors exp tion of num flammator stress responses [16]. In contrast to its transitory activation normal growth-signal transduction, NF-jB is constitutivel vated in a variety of leukemia and solid tumors, including lun cer. The constitutively activated NF-jB signaling pathway plays a critical role in promoting the survival and growth of tumor cells [17–24], but the molecular events that trigger this in lung cancer cells remains unclear. Ca2+/calmodulin-dependent kinase II (CaMKII) is a multifunc-tional serine/threonine kinase regulated through Ca2+ signaling [25]. There are four CaMKII homologous each encoded by distinct ⇑Corresponding authors. Address: Department of Respiratory Medicine, the Second Afï¬ liated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China. Tel.:+ 86 13957158572 (K. Wang). Address: Cancer Institute, the Second Afï¬ liated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China (R. Xu). E-mail addresses:[email protected](R. Xu),[email protected](K. Wang). Cancer Letters 344 (2014) 119–128 Contents lists availab Cancer L journal homepage: www. el R T1 S. Chai and Y. Qian contributed equally to this work. the kinase domain of the epidermal growth factor receptor (EGFR) gene and its corresponding targeted therapies have had a profound impact on NSCLC patient survival [2–4]. The introduction of EGFR tyrosine kinase inhibitors in advanced NSCLC patients with EGFR mutations greatly improved the response rate and progression-free lighting the need for the discovery of new thera NSCLC. NF-jB is a family of eukaryotic transcription in virtually all cell types, implicated in the regula genes, and is a central mediator of immune, in E0304-3835/$-see front matter 2013 Elsevier Ireland Ltd. All rights reserved. http://dx. doi. org/10.1016/j. canlet. 2013.10. 022ressed erous y, and during y acti-g can-NF-jB Therapeutic target 1. Introduction Lung cancer is the leading cause of cancer-related deaths world-wide. Non-small cell lung cancer (NSCLC) accounts for 75–85% of newly diagnosed lung cancers and its incidence is increasing glob-ally. Moreover, over 70% of NSCLC patients present with advanced disease, and the 5-year survival rate for NSCLC is only 16%[1]. Dur-other important milestone in the era of molecular targeted therapy for NSCLC [8, 9]. The response rate of the ALK inhibitor Crizotinib was up to 50% and 61% from 255 ALK-rearranged NSCLC patients enrolled in two single-arm trials [10]. However, as demonstrated by IPASS, even among a clinically deï¬ ned NSCLC patient cohort, only slightly more than half of these patients harbored activating EGFR mutations [11, 12]. Moreover, resistance to EGFR tyrosine ki-TR articleinfo Article history: Received 16 September 2013 Received in revised form 22 October 2013 Accepted …