EIF3H interacts with PDCD4 enhancing lung adenocarcinoma cell metastasis.
Yingying Hu, Wei Xiao, Yumin Lv, Xin Xie, Yang Liu, Jingjing He, Xingyu Tao, Yuting Ma, Yun Su, Liyang Wu, Weiyi Fang, Zhen Liu
Abstract
as well as metastasis in nude mice by activating epithelial-mesenchymal transition (EMT) signaling. Conversely, EIF3H knockdown with small interfering RNAs reversed these changes in LUAD cells. Furthermore, we discovered that introduction of PDCD4 to EIF3H-overexpressing LUAD cells abrogated the function of EIF3H, reducing migration and invasion of LUAD cells by downregulating EMT signaling. Taken together, our findings identified a previously unknown negative regulation of PDCD4 on EIF3H and confirmed EIF3H as an oncogenic factor in LUAD by enhancing EMT signaling, which was abrogated by PDCD4.
Topics & Concepts
Cancer researchGene knockdownAdenocarcinomaCarcinogenesisBiologyMetastasisSignal transductionTumor progressionCancerCell biologyGeneGeneticsBiochemistryCancer-related molecular mechanisms researchRNA modifications and cancerRNA Research and Splicing