ArticleJournal of experimental & clinical cancer research : CR2019
LPCAT1 promotes brain metastasis of lung adenocarcinoma by up-regulating PI3K/AKT/MYC pathway.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 2 of them syntheses that pooled it.
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Who cites it
105 citing papers in PubMed, 2 syntheses or guidelines pooled it, 164 citations in OpenAlex.
- Risk factors for brain metastasis in lung cancer: an umbrella review of systematic reviews and meta-analyses.BMJ open · 2025Pooled it
- Pooled it
- CDS2 Drives Tumor Progression in Epithelial Ovarian Cancer via the PI3K/AKT Pathway.Cancer medicine · 2026Article
- CDC20 promotes prostate cancer progression via modulating c-MYC and PI3K-AKT signaling.iScience · 2026Article
- Transcriptomic profiling of an in vivo diffuse large B-cell lymphoma model reveals molecular programs underlying CNS dissemination.Annals of hematology · 2026Article
- TRIM33 Reverses Cisplatin Resistance in Non-Small Cell Lung Cancer by Regulating the PI3K/AKT Pathway via Ubiquitination-Mediated Degradation of LPCAT1.World journal of oncology · 2026Article
- YY1-induced upregulation of DLGAP5 promotes tumor progression in lung adenocarcinoma via Wnt/β-catenin/EMT pathway.Journal of translational medicine · 2026Article
- Article
- The evolving landscape of brain metastasis: volume II.Trends in cancer · 2026Review
- LPCAT1 as a prognostic biomarker and risk indicator for hepatocellular carcinoma: insights into genes related to lipid metabolism.Frontiers in oncology · 2026Article
- Insights into extracellular vesicle-based platforms on the way to cancer treatment.Journal of translational medicine · 2025Review
- HMGB3 promotes brain metastasis of lung adenocarcinoma by recruiting SSBP1 for nuclear translocation to remodel mitochondrial metabolism.Cancer communications (London, England) · 2025Article
- ATP6V0D2 drives triple-negative breast cancer progression and inhibits cisplatin sensitivity by promoting PHLPP2 lysosomal degradation.iScience · 2025Article
- Exploring the evolutionary conservation and functional implications of Endothelin Converting Enzyme 1 (ECE1) in lamprey (Lethenteron reissneri).Fish physiology and biochemistry · 2025Article
- SET8 modulates prognosis and radiotherapeutic efficacy by regulating radiation-induced migration in lung adenocarcinoma.Journal of translational medicine · 2025Article
- Observational
- Association ofBiomedicines · 2025Article
- Metabolic adaptations of brain metastasis.Nature reviews. Cancer · 2025Review
- Prediction of biomarkers for brain metastasis in nonsmall cell lung cancer based on transcriptome sequencing.Medicine · 2025Article
- Overview of Preclinical and Clinical Trials of Nanoparticles for the Treatment of Brain Metastases.Pharmaceutics · 2025Review
45 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundBrain metastasis (BM) is associated with poor prognosis, recurrence, and death in patients with non-small cell lung cancer (NSCLC). Lysophosphatidylcholine acyltransferase 1 (LPCAT1) has been reported to be involved in the progression, metastasis and recurrence of malignancies. However, the potential role of LPCAT1 in NSCLC remains poorly understood. This study was aimed to identify genes involved in lung adenocarcinoma (LUAD) brain metastasis, and look into the role of LPCAT1 in LUAD progression.
methodsWe used integrative genomic analysis to identify genes involved in lung adenocarcinomas. LPCAT1 expression was evaluated in tumor tissues from LUAD patients and LUAD cell lines. The role of LPCAT1 was subsequently investigated both in vitro and in vivo. The mechanism underlying the involvement of LPCAT1 in LUAD progression was explored with the activator of PI3K/AKT pathway. RNA sequencing was performed to confirm the involvement of LPCAT1 and associated pathway in LUAD brain metastasis.
resultsLPCAT1 was up-regulated in LUAD tissues and cell lines. shRNA-mediated depletion of LPCAT1 not only abrogated cell proliferation, migration and invasion in vitro, but also arrested tumor growth and brain metastases in vivo. Notably, LPCAT1 at least partially influenced LUAD progression through PI3K/AKT signal pathway by targeting MYC transcription. Moreover, expression of LPCAT1 was higher in tissues of LUAD patients with BM than those without BM as revealed by IHC staining, RNA-Sequencing and qPCR analysis. Finally, elevated LPCAT1 expression in patients with lung adenocarcinomas was associated with a poor clinical outcome.
conclusionsThis study showed that LPCAT1 works as a regulator of cell metastasis and may serve as a novel therapeutic target for BM in lung adenocarcinoma.
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