ArticleExperimental and therapeutic medicine2016
Oncogenic role of epithelial cell transforming sequence 2 in lung adenocarcinoma cells.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Upregulated N-cadherin expression is associated with poor prognosis in epithelial-derived solid tumours: A meta-analysis.European journal of clinical investigation · 2018Pooled it
- Epithelial cell transforming 2 is regulated by Yes-associated protein 1 and mediates pancreatic cancer progression and metastasis.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- ECT2 promotes lung adenocarcinoma progression through extracellular matrix dynamics and focal adhesion signaling.Cancer science · 2021Article
- Effect of Ect2 Expression on the Growth of Triple-Negative Breast Cancer Cells with Paclitaxel Intervention.OncoTargets and therapy · 2020Article
- The role of contextual signal TGF-β1 inducer of epithelial mesenchymal transition in metastatic lung adenocarcinoma patients with brain metastases: an update on its pathological significance and therapeutic potential.Contemporary oncology (Poznan, Poland) · 2019Review
- P53 and Protein Phosphorylation Regulate the Oncogenic Role of Epithelial Cell Transforming 2 (ECT2).Medical science monitor : international medical journal of experimental and clinical research · 2017Article
Corrections and comments
- Retraction · 2021-05-21Duplication of Data · Investigation by Third Party · Paper Mill ·
- Retracted
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma, which is the most common non-small cell lung cancer, is the leading cause of death from cancer worldwide. Epithelial cell transforming sequence 2 (ECT2) is frequently upregulated and acts as an oncogene in various human cancers. In addition, ECT2 was reported to be upregulated in early stage lung adenocarcinoma. However, the detailed role of ECT2 in mediating the malignant phenotypes of lung adenocarcinoma cells has not previously been elucidated. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to examine ECT2 mRNA and protein expression levels, respectively. MTT, wound healing and Transwell assays were conducted to determine cell proliferation, migration and invasion abilities, respectively. In the present study, ECT2 was significantly upregulated in lung adenocarcinoma cell lines (H650, EKVX, HCC4006, HCC827, HCC2935, Hop62 and A549), as compared with a normal lung epithelial cell line (BEAS-2B). Moreover, knockdown of ECT2, induced by transfection with ECT2 siRNA, significantly inhibited the proliferation of lung adenocarcinoma A549 cells, whereas overexpression of ECT2 enhanced A549 cell proliferation. Furthermore, knockdown of ECT2 expression suppressed the migration and invasion of A549 cells, whereas overexpression of ECT2 enhanced the migration and invasion abilities of A549 cells. Notably, inhibition of ECT2 also suppressed the expression levels of N-cadherin and vimentin, whereas it enhanced the expression level of E-cadherin, indicating that ECT2 is associated with the epithelial-mesenchymal transition in A549 cells. On the contrary, overexpression of ECT2 enhanced the expression levels of N-cadherin and vimentin, whereas it reduced the expression level of E-cadherin in A549 cells. In conclusion, the results of the present study suggest that ECT2 has an oncogenic role in lung adenocarcinoma cells. Therefore, ECT2 may be a potential novel target for the treatment of lung adenocarcinoma.
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Registered trials
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