LINC00152 induced by TGF-β promotes metastasis via HuR in lung adenocarcinoma.
Wei XuLinna ChenJiheng LiuZhezhe ZhangRanran WangQianqian ZhangHuiting LiJuanjuan XiangLi FangPing XuZheng LiPublished in: Cell death & disease (2022)
Lung adenocarcinoma (LUAD) is one of the main causes of cancer-related mortality, with a strong tendency to metastasize early. Transforming growth factor-β (TGF-β) signaling is a powerful regulator to promote metastasis of LUAD. Here, we screened long non-coding RNAs (lncRNAs) responsive to TGF-β and highly expressed in LUAD cells, and finally obtained our master molecular LINC00152. We proved that the TGF-β promoted transcription of LINC00152 through the classical TGF-β/SMAD3 signaling pathway and maintained its stability through the RNA-binding protein HuR. Moreover, LINC00152 increased ZEB1, SNAI1 and SNAI2 expression via increasing the interactions of HuR and these transcription factors, ultimately promoting epithelial-mesenchymal transition of LUAD cell and enhancing LUAD metastasis in vivo. These data provided evidence that LINC00152 induced by TGF-β promotes metastasis depending HuR in lung adenocarcinoma. Designing targeting LINC00152 and HuR inhibitors may therefore be an effective therapeutic strategy for LUAD treatment.
Keyphrases
- transforming growth factor
- long non coding rna
- epithelial mesenchymal transition
- binding protein
- poor prognosis
- signaling pathway
- long noncoding rna
- cell proliferation
- transcription factor
- induced apoptosis
- cancer therapy
- type diabetes
- electronic health record
- cardiovascular disease
- big data
- single cell
- oxidative stress
- coronary artery disease
- bone marrow
- stem cells
- pi k akt
- cell therapy
- artificial intelligence
- dna binding
- smoking cessation