Nuclear export protein CSE1L interacts with P65 and promotes NSCLC growth via NF-κB/MAPK pathway
Heping Lin, Jing Li, Dandan Cheng, Xiaoling Zhang, Tao Yu, Fengdong Zhao, Qing Geng, M.X. Zhu, Hualei Kong, H. Li, Min Yao
Abstract
gain- and loss-of-function experiments, we found that CSE1L can promote NSCLC cell proliferation while inhibiting cell apoptosis. Through immunoprecipitation and mass spectrometry experiments, we demonstrated that CSE1L interacted with RELA (named as P65) and affected its location in the nucleus. Moreover, we found that one of the mechanisms by which CSE1L promotes proliferation and inhibits apoptosis is through activating the nuclear factor-κB (NF-κB)/mitogen-activated protein kinase (MAPK) signaling pathway. In summary, our findings indicated an oncogenic role of CSE1L in NSCLC tumorigenesis.
Topics & Concepts
CarcinogenesisDownregulation and upregulationImmunoprecipitationCancer researchCell growthMAPK/ERK pathwayLung cancerNuclear proteinMetastasisSignal transductionApoptosisProtein kinase AIn vivoBiologyKinaseCancerMedicineCell biologyPathologyGeneInternal medicineGeneticsTranscription factorNuclear Structure and FunctionRNA Research and SplicingCell death mechanisms and regulation