ArticleMetabolomics : Official journal of the Metabolomic Society2019
UPLC-MS-based metabolomics reveals metabolic dysregulation in ALDH1A1-overexpressed lung adenocarcinoma cells.
Article in Metabolomics : Official journal of the Metabolomic Society, 2019. 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.
- Article
- Huang-qin decoction increases the sensitivity of EGFR-TKIs to NSCLC cells by regulating stat3/GPX4 to induce redox ratio and ROS to inhibit CSCs.Journal of traditional and complementary medicine · 2026Article
- Targeted metabolomics reveals tricarboxylic acid cycle-related metabolites serve as predictive biomarkers for trastuzumab resistance in human epidermal growth factor receptor 2-positive breast cancer.Journal of molecular medicine (Berlin, Germany) · 2025Article
- CRISPR/Cas9 Targeting of Aldehyde Dehydrogenase 1A1 Reveals Heterogeneous Roles in Radiation Response and Redox Stress Across Clonal Lines in Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Article
- The Significance of Aldehyde Dehydrogenase 1 in Cancers.International journal of molecular sciences · 2024Review
- Article
- ALDH1A1 promotes PARP inhibitor resistance by enhancing retinoic acid receptor-mediated DNA polymerase θ expression.NPJ precision oncology · 2023Article
- Xanthine dehydrogenase rewires metabolism and the survival of nutrient deprived lung adenocarcinoma cells by facilitating UPR and autophagic degradation.International journal of biological sciences · 2023Article
- The KRAS-G12D mutation induces metabolic vulnerability in B-cell acute lymphoblastic leukemia.iScience · 2022Article
- ALDH1A1 in Cancers: Bidirectional Function, Drug Resistance, and Regulatory Mechanism.Frontiers in oncology · 2022Review
- ALDH1: A potential therapeutic target for cancer stem cells in solid tumors.Frontiers in oncology · 2022Review
- A Review on the Health Effects of Pesticides Based on Host Gut Microbiome and Metabolomics.Frontiers in molecular biosciences · 2021Review
- Whole-transcriptome Analysis of Fully Viable Energy Efficient Glycolytic-null Cancer Cells Established by Double Genetic Knockout of Lactate Dehydrogenase A/B or Glucose-6-Phosphate Isomerase.Cancer genomics & proteomicsArticle
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Authors and funding
6 authors.
Funding
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Abstract
introductionSpecific oncogenotypes can produce distinct metabolic changes in cancer. Recently it is considered that metabolic reprograming contributes heavily to drug resistance. Aldehyde dehydrogenase 1A1 (ALDH1A1), is overexpressed in drug resistant lung adenocarcinomas and may be the cause of acquired drug resistance. However, how ALDH1A1 affects metabolic profiling in lung adenocarcinoma cells remains elusive.
objectiveWe sought to investigate metabolic alterations induced by ALDH1A1 in lung adenocarcinoma in order to better understand the reprogramming and metabolic mechanism of resistance induced by ALDH1A1.
methodsMetabolic alterations in lung adenocarcinoma HCC827-ALDH1A1 cells were analyzed by ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS). HCC827-ALDH1A1 metabolic signatures were extracted by univariate and multivariate statistical analysis. Furthermore, metabolite enrichment analysis and pathway analysis were performed using MetaboAnalyst 4.0 software.
resultsTwenty-two metabolites were positively identified using authentic standards, including uridine monophosphate (UMP), uridine diphosphate (UDP), adenosine diphosphate (ADP), malic acid, malonyl-coenzyme A, nicotinamide adenine dinucleotide (NAD), coenzyme A and so on. Furthermore, metabolic pathway analysis revealed several dysregulated pathways in HCC827-ALDH1A1 cells, including nucleotide metabolism, urea cycle, tricarboxylic acid (TCA) cycle, and glycerol phospholipid metabolism etc.
conclusionLung cancer is the most frequent cause of cancer-related deaths worldwide. Nearly all patients eventually undergo disease progression due to acquired resistance. Mechanisms of biological acquired resistance need to be identified. Our study identified altered metabolites in HCC827-ALDH1A1 cells, enhancing our knowledge of lung adenocarcinoma metabolic alterations induced by ALDH1A1, creating a novel therapeutic pathway. These metabolic signatures of ALDH1A1 overexpression may shed light on molecular mechanisms in drug-resistant tumors, and on candidate drug targets. Furthermore, new molecular targets may provide the foundation for potential anticancer strategies for lung cancer therapy.
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