RETRACTED: Therapeutic potential of IBP as an autophagy inducer for treating lung cancer via blocking PAK1/Akt/mTOR signaling
Huimin Bu, Shirui Tan, Bo Yuan, Xiaomei Huang, Jiebang Jiang, Yejiao Wu, Jihong Jiang, Rongpeng Li
Abstract
. Mechanistically, IBP specifically promotes ubiquitination-mediated degradation of PAK1 (p21-activated kinase 1) and blocks its downstream Akt1/mTOR signaling pathway, leading to increased autophagic flux. In lung cancer xenografts in mice, IBP-induced cytostatic autophagy suppresses tumor development. Through site-directed mutational analysis, the underlying signaling augments ubiquitination via PAK1-ubiquitin interaction. Collectively, this work unravels the molecular mechanism underpinning IBP-induced cytostatic autophagy in lung cancer and characterizes IBP as a potential therapeutic agent for lung cancer treatment.
Topics & Concepts
AutophagyPI3K/AKT/mTOR pathwayLung cancerCancer researchPAK1CancerUbiquitinBiologyProtein kinase BCancer cellKinaseSignal transductionMedicineCell biologyApoptosisPathologyBiochemistryGeneticsGeneAutophagy in Disease and TherapyUbiquitin and proteasome pathwaysPolyamine Metabolism and Applications