ArticleOncology research2022
lncCRLA Enhanced Chemoresistance in Lung Adenocarcinoma That Underwent EpithelialMesenchymal Transition.
Article in Oncology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Long non-coding RNAs in tuberculosis: Immune regulation and clinical biomarker potential.iScience · 2026Review
- Liquid-liquid phase separation-driven regulated cell death: from molecular mechanisms to therapeutic strategies.Cell death discovery · 2026Review
- Lung Cancer Chemoresistance: Insights into the Regulatory Role of lncRNAs.Cancer management and research · 2026Review
- METTL16 accelerates lung adenocarcinoma progression by inducing N6-methyladenosine modification of GTSE1 to regulate p53 pathway and cell cycle.Cell division · 2025Article
- Significance ofFrontiers in pharmacology · 2025Article
- The fate and function of non-coding RNAs during necroptosis.Epigenomics · 2024Review
- Long non-coding RNAs in ferroptosis, pyroptosis and necroptosis: from functions to clinical implications in cancer therapy.Frontiers in oncology · 2024Review
- The GJB3 correlates with the prognosis, immune cell infiltration, and therapeutic responses in lung adenocarcinoma.Open medicine (Warsaw, Poland) · 2024Article
- Drug resistance related genes in lung adenocarcinoma predict patient prognosis and influence the tumor microenvironment.Scientific reports · 2023Article
- LncRNA NR_003508 SuppressesInternational journal of molecular sciences · 2023Article
- The regulation of necroptosis and perspectives for the development of new drugs preventing ischemic/reperfusion of cardiac injury.Apoptosis : an international journal on programmed cell death · 2022Review
- Article
- Risk coefficient model of necroptosis-related lncRNA in predicting the prognosis of patients with lung adenocarcinoma.Scientific reports · 2022Article
- Clinicopathological and Prognostic Value of Necroptosis-Associated lncRNA Model in Patients with Kidney Renal Clear Cell Carcinoma.Disease markers · 2022Article
- Macrophage Infiltration Initiates RIP3/MLKL-Dependent Necroptosis in Paclitaxel-Induced Neuropathic Pain.Mediators of inflammation · 2022Article
- Identification of Prognostic Signature of Necroptosis-Related lncRNAs and Molecular Subtypes in Glioma.Computational and mathematical methods in medicine · 2022Article
- Necroptosis Identifies Novel Molecular Phenotypes and Influences Tumor Immune Microenvironment of Lung Adenocarcinoma.Frontiers in immunology · 2022Article
- Predicting Prognosis and Distinguishing Cold and Hot Tumors in Bladder Urothelial Carcinoma Based on Necroptosis-Associated lncRNAs.Frontiers in immunology · 2022Article
Corrections and comments
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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
EMT confers increased metastatic potential and the resistance to chemotherapies to cancer cells. However, the precise mechanisms of EMT-related chemotherapy resistance remain unclear. c-Src-mediated caspase 8 phosphorylation essential for EMT in lung adenocarcinoma cell lines preferentially occurs in cells with the mesenchymal phenotype, resulting in chemoresistance to cisplatin plus paclitaxel in patients with resectable lung adenocarcinoma and a significantly worse 5-year PFS. Cisplatin killed lung adenocarcinoma cells regardless of caspase 8. Paclitaxel-triggered necroptosis in lung adenocarcinoma cells was dependent on the phosphorylation or deficiency of caspase 8, during which FADD interacted with RIPK1 to activate the RIPK1/RIPK3/MLKL signaling axis. Accompanied with c-Src-mediated caspase 8 phosphorylation to trigger EMT, a novel lncRNA named lncCRLA was markedly upregulated and inhibited RIPK1-induced necroptosis by impairing RIPK1RIPK3 interaction via binding to the intermediate domain of RIPK1. Dasatinib mitigated c-Src-mediated phosphorylation of caspase 8-induced EMT and enhanced necroptosis in mesenchymal-like lung adenocarcinoma cells treated with paclitaxel, while c-FLIP knockdown predominantly sensitized the mesenchymal-like lung adenocarcinoma cells to paclitaxel+dasatinib. c-Srccaspase 8 interaction initiates EMT and chemoresistance via caspase 8 phosphorylation and lncCRLA expression, to which the dasatinib/paclitaxel liposome+siFLIP regimen was lethal.
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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.