ArticleProceedings of the National Academy of Sciences of the United States of America2008
Down-regulation of 14-3-3zeta suppresses anchorage-independent growth of lung cancer cells through anoikis activation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 144 citations in OpenAlex.
- Exploring 14-3-3ζ: insights into its role in cancer mechanisms and future therapeutic applications.Hereditas · 2026Review
- Metabolic reprogramming and signaling adaptations in anoikis resistance: mechanisms and therapeutic targets.Molecular and cellular biochemistry · 2025Review
- Differences of genomic alterations and heavy metals in non-small cell lung cancer with different histological subtypes.Journal of cancer research and clinical oncology · 2023Article
- Loss of ubiquitin-specific peptidase 18 destabilizes 14-3-3ζ protein and represses lung cancer metastasis.Cancer biology & therapy · 2022Article
- Review
- SGK2, 14-3-3, and HUWE1 Cooperate to Control the Localization, Stability, and Function of the Oncoprotein PTOV1.Molecular cancer research : MCR · 2022Article
- Toxicity and Anti-Proliferative Properties ofLife (Basel, Switzerland) · 2021Article
- The 14-3-3σ protein promotes HCC anoikis resistance by inhibiting EGFR degradation and thereby activating the EGFR-dependent ERK1/2 signaling pathway.Theranostics · 2021Article
- Down-regulation of 14-3-3zeta reduces proliferation and increases apoptosis in human glioblastoma.Cancer gene therapy · 2020Article
- 14-3-3ζ binds to and stabilizes phospho-beclin 1Journal of cellular and molecular medicine · 2020Article
- The role of YWHAZ in cancer: A maze of opportunities and challenges.Journal of Cancer · 2020Review
- [14-3-3ζ protein mediates gemcitabine resistance in NK/T-cell lymphoma].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Article
- 14-3-3ζ binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells.Cancer medicine · 2018Article
- Review
- Effect of cytokine-induced killer cells combined with dendritic cells on the survival rate and expression of 14-3-3ζ and p-Bad proteins in Lewis lung cancer cell lines.Oncology letters · 2018Article
- Overexpression of 14-3-3ζ in lung tissue predicts an improved outcome in patients with lung adenocarcinoma.Oncology letters · 2018Article
- 14-3-3β exerts glioma-promoting effects and is associated with malignant progression and poor prognosis in patients with glioma.Experimental and therapeutic medicine · 2018Article
- 14-3-3ζ binds the proteasome, limits proteolytic function and enhances sensitivity to proteasome inhibitors.Leukemia · 2018Article
- 14-3-3ζ Overexpression is Associated with Poor Prognosis in Ovarian Cancer.Yonsei medical journal · 2018Article
- 14-3-3ζ loss leads to neonatal lethality by microRNA-126 downregulation-mediated developmental defects in lung vasculature.Cell & bioscience · 2017Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The family of 14-3-3 proteins has emerged as critical regulators of diverse cellular responses under both physiological and pathological conditions. Here, we report an important role of 14-3-3zeta in tumorigenesis through a mechanism that involves anoikis resistance. 14-3-3zeta is up-regulated in a number of cancer types, including lung cancer. Through an RNAi approach using human lung adenocarcinoma-derived A549 cells as a model system, we have found that knockdown of a single zeta isoform of 14-3-3 is sufficient to restore the sensitivity of cancer cells to anoikis and impair their anchorage-independent growth. Enhanced anoikis appears to be mediated in part by up-regulated BH3-only proteins, Bad and Bim, coupled with decreased Mcl-1, resulting in the subsequent activation of Bax. This study suggests a model in which anchorage-independent growth of lung cancer cells requires the presence of 14-3-3zeta. This work not only reveals a critical role of 14-3-3zeta in anoikis suppression in lung cancer cells, but also identifies and validates 14-3-3zeta as a potential molecular target for anticancer therapeutic development.
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Registered trials
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