ArticleMolecular medicine reports2019
EVI‑1 acts as an oncogene and positively regulates calreticulin in breast cancer.
Article in Molecular medicine reports, 2019. 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 It has been retracted, and should not be counted.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 8 papers.
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
8 citing papers in PubMed, 10 citations in OpenAlex.
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- Calreticulin as a marker and therapeutic target for cancer.Clinical and experimental medicine · 2023Review
- CRISPR-mediated MECOM depletion retards tumor growth by reducing cancer stem cell properties in lung squamous cell carcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Effects of Pubertal Exposure to Butyl Benzyl Phthalate, Perfluorooctanoic Acid, and Zeranol on Mammary Gland Development and Tumorigenesis in Rats.International journal of molecular sciences · 2022Article
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Corrections and comments
- Retraction · 2023-10-09Author Unresponsive · Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image · Euphemisms for Duplication · Euphemisms for Plagiarism · Plagiarism of Data · · see also: https://pubpeer.com/publications/406C48C4599B3C47EB31B092D81465
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ecotropic viral integration site‑1 (EVI‑1) is an important transcription factor involved in oncogenesis. Aberrant EVI‑1 expression has been reported to be a characteristic of multiple types of malignancies; however, very little is known about how EVI‑1 regulates breast cancer. Current knowledge of how target genes mediate the biological function of EVI‑1 remains limited. In the present study, overexpression of EVI‑1 promoted cell proliferation, migration, and invasion, and inhibited apoptosis in breast cancer. By contrast, silencing of EVI‑1 inhibited cell proliferation, migration and invasion, and enhanced apoptosis in breast cancer. In addition, the results also revealed that the aberrant expression of EVI‑1 regulates genes associated with the apoptotic pathway in breast cancer. Furthermore, EVI‑1 was also likely to target the promoter region of calreticulin (CRT) in vitro. It was concluded that EVI‑1 can affect epithelial mesenchymal transition‑associated genes by regulating the expression of CRT in breast cancer. The results revealed that EVI‑1 may be a potential effective therapeutic target in breast cancer.
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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.