ArticleOncotarget2016
Loss of Par3 promotes lung adenocarcinoma metastasis through 14-3-3ζ protein.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- The polarity protein Par3 enhances renal cell carcinoma metastasisCancer biology & medicine · 2025Article
- Inhibition of Pard3 promotes breast cancer metastasis via the USP28 mediated deubiquitination of Snail1.Heliyon · 2023Article
- Echinocystic acid induces the apoptosis, and inhibits the migration and invasion of non-small cell lung cancer cells.Medical oncology (Northwood, London, England) · 2023Article
- Loss of ubiquitin-specific peptidase 18 destabilizes 14-3-3ζ protein and represses lung cancer metastasis.Cancer biology & therapy · 2022Article
- lncRNA NEAT1 Downregulation Ameliorates the Myocardial Infarction of Mice by Regulating the miR-582-5p/F2RL2 Axis.Cardiovascular therapeutics · 2022Article
- Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022Review
- The polarity protein PARD3 and cancer.Oncogene · 2021Review
- High expression of PARD3 predicts poor prognosis in hepatocellular carcinoma.Scientific reports · 2021Article
- Investigation and Functional Enrichment Analysis of the Human Host Interaction Network with Common Gram-Negative Respiratory Pathogens Predicts Possible Association with Lung Adenocarcinoma.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Article
- MiRNA-1225 Inhibits Osteosarcoma Tumor Growth and Progression by Targeting YWHAZ.OncoTargets and therapy · 2021Article
- The role of YWHAZ in cancer: A maze of opportunities and challenges.Journal of Cancer · 2020Review
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Partitioning defective protein 3 (Par3) can activate the Tiam1/Rac pathway to inhibit invasion and metastasis in many cancers; however, the role of Par3 in lung adenocarcinoma remains unknown. Here we show that Par3 is downregulated in lung adenocarcinoma tissues and is associated with higher rates of lymph node metastasis and recurrence. Our functional study demonstrated that knock-down of Par3 promoted lung adenocarcinoma cell growth, cell migration, tumor formation, and metastasis, all of which were effectively inhibited when 14-3-3ζ was silenced. We found that Par3 binded with 14-3-3ζ protein and also showed that Par3 abrogated the binding of 14-3-3ζ to Tiam1, which was responsible for Rac1 activation. Knock-down of 14-3-3ζ inhibited Tiam1/Rac-GTP activation and blocked the invasive behavior of cells lacking Par3. These data suggest that loss of Par3 promotes metastatic behavior in lung adenocarcinoma cells through 14-3-3ζ protein.
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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.