ArticleBiology direct2024
PLAU promotes growth and attenuates cisplatin chemosensitivity in ARID1A-depleted non-small cell lung cancer through interaction with TM4SF1.
Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- Integrating Single-Cell, Bulk, and Spatial Transcriptomics Unveils a Novel Ribosome Biogenesis-Related Prognostic Model and DefinesInternational journal of molecular sciences · 2026Article
- RIP kinase inhibition with Necrostatin-1 improves human marginal mass islet graft survival and function for the management of type 1 diabetes.Cell death & disease · 2026Article
- MicroRNA-663a upregulation upon ARID1A depletion promotes the growth and migration of esophageal cancer cells by targeting FKBP8.Translational cancer research · 2026Article
- Identification of novel ceRNA networks associated with system hemostasis and their prognostic implication in lung squamous cell carcinoma.Journal of thrombosis and thrombolysis · 2026Article
- Single-Cell and Multiomic Analysis Reveals Neutrophil Heterogeneity and Prognostic Value in Cervical Lesions.Cancer science · 2026Article
- Exosomal FOSL1 From Cancer-associated Fibroblasts Drives the Progression and Pro-tumorigenic M2 Macrophage Polarization of Hepatocellular Carcinoma By Activating PLAU Transcription.Applied biochemistry and biotechnology · 2026Article
- Downregulated PLAU alleviates acute rejection after liver transplantation by targeting Ptgs2 in macrophages.Frontiers in immunology · 2026Article
- Baicalein inhibits the progression of thyroid cancer by suppressing the TPL2/MEK2/ERK2 pathway.Frontiers in endocrinology · 2026Article
- Exploring medicinal mechanism of baicalin in tumor microenvironment of melanoma via bioinformatic and in vitro study.Medical oncology (Northwood, London, England) · 2025Article
- ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5.BMC pulmonary medicine · 2025Article
- Interpretable artificial intelligence based on immunoregulation-related genes predicts prognosis and immunotherapy response in lung adenocarcinoma.Frontiers in bioinformatics · 2025Article
- Development and validation of an ARID1A-related immune genes risk model in evaluating prognosis and immune therapeutic efficacy for gastric cancer patients: a translational study.Frontiers in immunology · 2025Article
- Identification of genetic associations between acute myocardial infarction and non-small cell lung cancer.Frontiers in molecular biosciences · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Loss of ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, contributes to malignant progression in multiple cancers including non-small cell lung cancer (NSCLC). In the search for key genes mediating the aggressive phenotype caused by ARID1A loss, we analyzed 3 Gene Expression Omnibus (GEO) datasets that contain RNA sequencing data from ARID1A-depleted cancer cells. PLAU was identified as a common gene that was induced in different cancer cells upon ARID1A depletion. Overexpression of PLAU positively modulated NSCLC cell growth, colony formation, cisplatin resistance, and survival under serum deprivation. Moreover, enforced expression of PLAU enhanced tumorigenesis of NSCLC cells in nude mice. Mechanistically, PLAU interacted with TM4SF1 to promote the activation of Akt signaling. TM4SF1-overexpressing NSCLC cells resembled those with PLAU overepxression. Knockdown of TM4SF1 inhibited the growth and survival and increased cisplatin sensitivity in NSCLC cells. The interaction between PLAU and TM4SF1 led to the activation of Akt signaling that endowed ARID1A-depleted NSCLC cells with aggressive properties. In addition, treatment with anti-TM4SF1 neutralizing antibody reduced the growth, cisplatin resistance, and tumorigenesis of ARID1A-depleted NSCLC cells. Taken together, PLAU serves as a target gene of ARID1A and promotes NSCLC growth, survival, and cisplatin resistance by stabilizing TM4SF1. Targeting TM4SF1 may be a promising therapeutic strategy for ARID1A-mutated NSCLC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.