ArticleOncology letters2017
MicroRNA-204 suppressed proliferation and motility capacity of human hepatocellular carcinoma via directly targeting zinc finger E-box binding homeobox 2.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- miR-204 suppresses cancer stemness and enhances osimertinib sensitivity in non-small cell lung cancer by targeting CD44.Molecular therapy. Nucleic acids · 2024Article
- Review
- miR‑498 inhibits the growth and metastasis of liver cancer by targeting ZEB2.Oncology reports · 2019Article
- MicroRNA-204 attenuates the migration and invasion of pancreatic cancer cells by targeting ZEB1/EMT axis.International journal of clinical and experimental pathology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal expression levels of microRNA-204 (miR-204) have been identified in various types of human cancer. However, the expression and functions of miR-204, and the underlying molecular mechanism involved in the initiation and progression of hepatocellular carcinoma (HCC), require further investigation. The results of the present study demonstrated that miR-204 is downregulated in HCC tissues and cell lines. Notably, zinc finger E-box binding homeobox 2 (ZEB2) was identified as a direct target of miR-204 in HCC. In addition, miR-204 negatively regulates ZEB2 expression level in HCC cells at the post-transcriptional level. In functional studies, the overexpression of miR-204 inhibited the proliferation, migration and invasion of HCC cells. Furthermore, the knockdown of ZEB2 may mimic the functions of miR-204 in HCC cells, suggesting that ZEB2 is a direct functional target of miR-204. In conclusion, the results of the present study indicated that miR-204 suppresses the tumor growth, migration and invasion of HCC cells by directly targeting ZEB2, and may serve as a novel therapeutic target for HCC.
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