ArticleClinical & experimental metastasis2020
Cullin 3 overexpression inhibits lung cancer metastasis and is associated with survival of lung adenocarcinoma.
Article in Clinical & experimental metastasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 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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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Protein neddylation in lung tumorigenesis: Target validation and targeted therapy.Fundamental research · 2025Review
- Knockdown of cullin 3 inhibits progressive phenotypes and increases chemosensitivity in cholangiocarcinoma cells.Molecular medicine reports · 2024Article
- Long non-coding RNA GNAS-AS1 knockdown inhibits proliferation and epithelial-mesenchymal transition of lung adenocarcinoma cells via the microRNA-433-3p/Rab3A axis.Open medicine (Warsaw, Poland) · 2023Article
- Role of NRF2 in Lung Cancer.Cells · 2021Review
- microRNA-130b-3p Contained in MSC-Derived EVs Promotes Lung Cancer Progression by Regulating the FOXO3/NFE2L2/TXNRD1 Axis.Molecular therapy oncolytics · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cullin 3 (CUL3), a molecular scaffold of Cullin-RING ubiquitin ligase, plays an important role in regulating biological processes through modulating the ubiquitylation and degradation of various protein substrates. Dysfunction of CUL3 is implicated in the development of several human diseases. However, the clinical significance and prognostic value of CUL3 in lung cancer have not been investigated. This study investigated the CUL3-modulating potential of non-small cell lung cancer cell lines, H1299, H358, H2170 and H520, by using immunoblotting, MTT, migration, invasion, colony formation and in vivo tumorigenicity assays. The prognostic significance of CUL3 was measured by public KM plotter database (http://kmplot.com/analysis/index.php?p=service&cancer=breast) and tissue immunohistochemistry analysis. The public online database analysis revealed that elevated mRNA expression of CUL3 was associated with better prognosis for non-small cell lung cancer and lung adenocarcinoma. In vitro experiments showed that ectopic overexpression of CUL3 significantly inhibited lung adenocarcinoma cell proliferation and migration, and the tumor-suppressive effect of CUL3 was dependent on the Nrf2/RhoA axis. In vivo mice model demonstrated that overexpression of CUL3 lead to a significant reduction of lung adenocarcinoma growth and metastasis. Importantly, tissue immunohistochemistry analysis showed that about 47% of non-small cell lung cancer tissues were expressed of CUL3 at high levels. Overexpression of CUL3 predicted favorable overall survival in non-small cell lung cancer patients, especially in lung adenocarcinoma, but not in lung squamous cell carcinoma patients. CUL3 could serve as a prognostic biomarker for lung adenocarcinoma. Loss of CUL3 might be driving tumorigenesis by activating the Nrf2/RhoA pathway.
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