ArticleAging2022
Overexpression of 14-3-3ζ primes disease recurrence, metastasis and resistance to chemotherapy by inducing epithelial-mesenchymal transition in NSCLC.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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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
7 citing papers in PubMed, 13 citations in OpenAlex.
- Clinical significance of serum levels of 14-3-3β protein in patients with non-small cell lung cancer.Scientific reports · 2026Article
- Exploring 14-3-3ζ: insights into its role in cancer mechanisms and future therapeutic applications.Hereditas · 2026Review
- Article
- The Interaction between miRNAs and 14-3-3ζ Protein in Different Diseases.Protein and peptide letters · 2025Review
- Sirt1 Overexpression Inhibits Fibrous Scar Formation and Improves Functional Recovery After Cerebral Ischemic Injury Through the Deacetylation of 14-3-3ζ.Molecular neurobiology · 2023Article
- Epithelial-mesenchymal transition is associated with osteopontin-induced EGFR‑TKI resistance in EGFR mutant non-small cell lung cancer.Journal of thoracic disease · 2023Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prognosis of non-small cell lung cancer (NSCLC) is disappointing because disease recurrence and distant metastasis inevitably occurred. The aim of the present study is to identify novel biomarkers predicting tumor recurrence and metastasis. The 14-3-3ζ protein has been extensively described as a tumor promoter in a panel of solid tumors, including NSCLC. However, there is a big gap regarding the knowledge between 14-3-3ζ and NSCLC recurrence. In this study, we found that overexpression of 14-3-3ζ was more frequent in NSCLC tumor tissues with tumor recurrence. By using scratch healing assay and transwell assay, we demonstrated that NSCLC cells with high expression of 14-3-3ζ gained increased motile and invasive capacity, whereas siRNA-mediated knockdown of endogenous 14-3-3ζ abrogated cancer cell dissemination. Intriguingly, we found that NSCLC cells underwent epithelial-mesenchymal transition (EMT) after the induction of 14-3-3ζ
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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.