ArticleBMC cancer2018
LC-MS based sphingolipidomic study on A549 human lung adenocarcinoma cell line and its taxol-resistant strain.
Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Decreased sphingomyelin (t34:1) is a candidate predictor for lung squamous cell carcinoma recurrence after radical surgery: a case-control study.BMC cancer · 2021Pooled it
- Biomarkers for non-small cell lung cancer risk using multi-omics approaches: a nested case-control study.Translational lung cancer research · 2025Article
- Sphingolipid metabolism dysregulation: A cause for lung cancer development, progression, and resistance to therapies.Chinese medical journal pulmonary and critical care medicine · 2025Review
- The antimicrobial activity of ETD151 defensin is dictated by the presence of glycosphingolipids in the targeted organisms.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeted lipidomics meets transcriptomics: how cinobufagin rewires fatty acid, sphingolipid, and glycerophospholipid metabolism to combat hepatoma cell growth.Frontiers in pharmacology · 2025Article
- ReTimeML: a retention time predictor that supports the LC-MS/MS analysis of sphingolipids.Scientific reports · 2024Article
- Rectal Cancer Tissue Lipidome Differs According to Response to Neoadjuvant Therapy.International journal of molecular sciences · 2023Article
- ECHS1, an interacting protein of LASP1, induces sphingolipid-metabolism imbalance to promote colorectal cancer progression by regulating ceramide glycosylation.Cell death & disease · 2021Article
- Sphingomyelin(d35:1) as a novel predictor for lung adenocarcinoma recurrence after a radical surgery: a case-control study.BMC cancer · 2020Observational
- Article
- Depletion of Host and Viral Sphingomyelin Impairs Influenza Virus Infection.Frontiers in microbiology · 2020Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundResistance to chemotherapy drugs (e.g. taxol) has been a major obstacle in successful cancer treatment. In A549 human lung adenocarcinoma, acquired resistance to the first-line chemotherapy taxol has been a critical problem in clinics. Sphingolipid (SPL) controls various aspects of cell growth, survival, adhesion, and motility in cancer, and has been gradually regarded as a key factor in drug resistance. To better understand the taxol-resistant mechanism, a comprehensive sphingolipidomic approach was carried out to investigate the sphingolipid metabolism in taxol-resistant strain of A549 cell (A549T).
methodsA549 and A549T cells were extracted according to the procedure with optimal condition for SPLs. Sphingolipidomic analysis was carried out by using an UHPLC coupled with quadrupole time-of-flight (Q-TOF) MS system for qualitative profiling and an UHPLC coupled with triple quadrupole (QQQ) MS system for quantitative analysis. The differentially expressed sphingolipids between taxol-sensitive and -resistant cells were explored by using multivariate analysis.
resultsBased on accurate mass and characteristic fragment ions, 114 SPLs, including 4 new species, were clearly identified. Under the multiple reaction monitoring (MRM) mode of QQQ MS, 75 SPLs were further quantified in both A549 and A549T. Multivariate analysis explored that the levels of 57 sphingolipids significantly altered in A549T comparing to those of A549 (p < 0.001 and VIP > 1), including 35 sphingomyelins (SMs), 14 ceramides (Cers), 3 hexosylceramides (HexCers), 4 lactosylceramides (LacCers) and 1 sphingosine. A significant decrease of SM and Cer levels and overall increase of HexCer and LacCer represent the major SPL metabolic characteristic in A549T.
conclusionsThis study investigated sphingolipid profiles in human lung adenocarcinoma cell lines, which is the most comprehensive sphingolipidomic analysis of A549 and A549T. To some extent, the mechanism of taxol-resistance could be attributed to the aberrant sphingolipid metabolism, "inhibition of the de novo synthesis pathway" and "activation of glycosphingolipid pathway" may play the dominant role for taxol-resistance in A549T. This study provides insights into the strategy for clinical diagnosis and treatment of taxol resistant lung cancer.
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