ArticleCell death & disease2022
SIX5-activated LINC01468 promotes lung adenocarcinoma progression by recruiting SERBP1 to regulate SERPINE1 mRNA stability and recruiting USP5 to facilitate PAI1 protein deubiquitylation.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 28 citations in OpenAlex.
- Lipid-Soluble Signaling Molecular Model Predicts Prognosis and Immunotherapy Response in Gastric Cancer.Lipids · 2026Article
- Exercise modulation of the alternative splicing landscape in human tissues.bioRxiv : the preprint server for biology · 2026Article
- Aristolochic acid I accelerates lung adenocarcinoma progression coupled with the upregulation of core oncogenic networks: an integrated network toxicology and experimental study.Frontiers in pharmacology · 2026Article
- Investigating the Cellular Responses to Combined Nisin and Urolithin B Treatment (7:3) in HKB-11 Lymphoma Cells.International journal of molecular sciences · 2025Article
- The role of RNA binding proteins in cancer biology: A focus on FMRP.Genes & diseases · 2025Review
- Article
- Identification the Tumor Mechanics-Related Biomarkers in Gastric Cancer Patients Based on Bioinformatics and Machine Learning.International journal of general medicine · 2025Article
- Adipsin improves diabetic hindlimb ischemia through SERPINE1 dependent angiogenesis.Cardiovascular diabetology · 2024Article
- FTO/m6A mediates miR-138-5p maturation and regulates gefitinib resistance of lung adenocarcinoma cells by miR-138-5p/LCN2 axis.BMC cancer · 2024Article
- KSHV vIL-6 promotes SIRT3-induced deacetylation of SERBP1 to inhibit ferroptosis and enhance cellular transformation by inducing lipoyltransferase 2 mRNA degradation.PLoS pathogens · 2024Article
- Unraveling the Mechanism of Action of Ubiquitin-Specific Protease 5 and Its Inhibitors in Tumors.Clinical Medicine Insights. Oncology · 2024Review
- Long Noncoding RNA ZBED5-AS1 Facilitates Tumor Progression and Metastasis in Lung Adenocarcinoma via ZNF146/ATR/Chk1 Axis.International journal of molecular sciences · 2023Article
- Construction and experimental validation of an acetylation-related gene signature to evaluate the recurrence and immunotherapeutic response in early-stage lung adenocarcinoma.BMC medical genomics · 2022Article
- Comprehensive analysis of the potential role and prognostic value of sine oculis homeobox homolog family in colorectal cancer.World journal of gastrointestinal oncology · 2022Article
- LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2.Cell death discovery · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing research has uncovered the involvement of long noncoding RNAs (lncRNAs) in the progression of multiple cancers including lung adenocarcinoma (LUAD). RT-qPCR and western blot were done to measure RNAs and proteins. Functional assays assessed LUAD cell biological behaviors under knockdown or overexpression of LINC01468, SIX5, SERBP1 or SERPINE1, and the specific function of those genes in regulating LUAD progression was evaluated via animal experiments. Supported by bioinformatics analysis, the interaction among genes was verified via mechanism assays. Upregulation of LINC01468 in LUAD tissues and cells as well as its association with poor clinical outcome was predicted. LINC01468, transcriptionally activated by SIX5, could strengthen proliferative, migratory and invasive abilities of LUAD cells. The oncogenic role of LINC01468 was further validated via animal experiments. SIX5 was a positive transcription regulator of LINC01468 and could exacerbate LUAD cell malignant behaviors. LINC01468 could recruit SERBP1 to enhance SERPINE1 mRNA stability and interact with USP5 to affect PAI1 protein ubiquitination. The oncogenic role of SERBP1 and SERPINE1 was also confirmed. Rescue experiments finally verified LINC01468 modulated proliferation, migration and invasion of LUAD cells via upregulation of SERPINE1. Our observations could contribute to deeper understanding of LUAD.
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