ArticleProteomics2014
Proteomic signatures associated with p53 mutational status in lung adenocarcinoma.
Article in Proteomics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Role of PGC-1α in the proliferation and metastasis of malignant tumors.Journal of molecular histology · 2025Review
- RETRACTED: High PGC-1α Expression as a Poor Prognostic Indicator in Intracranial Glioma.Biomedicines · 2024Article
- [EHHADH is a key gene in fatty acid metabolism pathways in hepatocellular carcinoma: a transcriptomic analysis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Synergistic Tumor Inhibition via Energy Elimination by Repurposing Penfluridol and 2-Deoxy-D-Glucose in Lung Cancer.Cancers · 2022Article
- Protein citrullination as a source of cancer neoantigens.Journal for immunotherapy of cancer · 2021Article
- SIRT1/PGC-1α/PPAR-γ Correlate With Hypoxia-Induced Chemoresistance in Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Review
- Review
- PGC-1α as a Pivotal Factor in Lipid and Metabolic Regulation.International journal of molecular sciences · 2018Review
- p53 and metabolism: from mechanism to therapeutics.Oncotarget · 2018Review
- Peroxisome Proliferator-Activated ReceptorPPAR research · 2018Review
- Functional variomics and network perturbation: connecting genotype to phenotype in cancer.Nature reviews. Genetics · 2017Review
- Role of CPS1 in Cell Growth, Metabolism and Prognosis in LKB1-Inactivated Lung Adenocarcinoma.Journal of the National Cancer Institute · 2017Article
- Functional characterization of AMP-activated protein kinase signaling in tumorigenesis.Biochimica et biophysica acta · 2016Review
- PGC-1 Coactivators: Shepherding the Mitochondrial Biogenesis of Tumors.Trends in cancer · 2016Review
- Repeated PM2.5 exposure inhibits BEAS-2B cell P53 expression through ROS-Akt-DNMT3B pathway-mediated promoter hypermethylation.Oncotarget · 2016Article
- F-BOX proteins in cancer cachexia and muscle wasting: Emerging regulators and therapeutic opportunities.Seminars in cancer biology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
p53 is commonly mutated in lung adenocarcinoma. Mutant p53 loses wild-type function and some missense mutations further acquire oncogenic functions, while p53 wild-type may also induce pro-survival signaling. Therefore identification of signatures based on p53 mutational status has relevance to our understanding of p53 signaling pathways in cancer and identification of new therapeutic targets. To this end, we compared proteomic profiles of three cellular compartments (whole-cell extract, cell surface, and media) from 28 human lung adenocarcinoma cell lines that differ based on p53 mutational status. In total, 11,598, 11,569, and 9090 protein forms were identified in whole-cell extract, cell surface, and media, respectively. Bioinformatic analysis revealed that representative pathways associated with epithelial adhesion, immune and stromal cells, and mitochondrial function were highly significant in p53 missense mutations, p53 loss and wild-type p53 cell lines, respectively. Of note, mRNA levels of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α), a transcription coactivator that promotes mitochondrial oxidative phosphorylation and mitochondrial biogenesis, was substantially higher in p53 wild-type cell lines compared to either cell lines with p53 loss or with missense mutation. Small interfering RNA targeting PGC1-α inhibited cell proliferation in p53 wild-type cell lines, indicative of PGC1-α and its downstream molecules as potential therapeutic targets in p53 wild-type lung adenocarcinoma.
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Registered trials
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.