ArticleIranian journal of basic medical sciences2016
miR-506 inhibits cell proliferation and invasion by targeting TET family in colorectal cancer.
Article in Iranian journal of basic medical sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Therapeutic potential of microRNA-506 in cancer treatment: mechanisms and therapeutic implications.Frontiers in oncology · 2025Review
- Vitamin C enhances co-localization of novel TET1 nuclear bodies with both Cajal and PML bodies in colorectal cancer cells.Epigenetics · 2024Article
- TET2 Is Downregulated in Early Esophageal Squamous Cell Carcinoma and Promotes Esophageal Squamous Cell Malignant Behaviors.Digestive diseases and sciences · 2024Article
- Regulation of DNA methylation machinery by epi-miRNAs in human cancer: emerging new targets in cancer therapy.Cancer gene therapy · 2021Review
- ChrXq27.3 miRNA cluster functions in cancer development.Journal of experimental & clinical cancer research : CR · 2021Review
- Crosstalk between cancer cells and tumor associated macrophages is required for mesenchymal circulating tumor cell-mediated colorectal cancer metastasis.Molecular cancer · 2019Article
- MiR-506 Suppresses Colorectal Cancer Development by Inhibiting Orphan Nuclear Receptor NR4A1 Expression.Journal of Cancer · 2019Article
- Review
- miR‑647 and miR‑1914 promote cancer progression equivalently by downregulating nuclear factor IX in colorectal cancer.Molecular medicine reports · 2017Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTen-eleven translocation (TET) family members have been shown to be involved in the development of many tumors. However, the biological role of the TET family and its mechanism of action in colorectal carcinogenesis and progression remain poorly understood. MATERIALS AND
methodsWe measured the expression levels of TET family members in colorectal cancer (CRC) specimens, in the corresponding normal tissues and in cell lines using quantitative real-time PCR (qRT-PCR) and in situ hybridization (ISH). Both the protein function and the protein-independent role of TETs were investigated by cell viability assays and cell invasion assays using in vitro and in vivo models.
resultsWe found that all three TET genes were strongly up-regulated at the transcript level in CRC samples compared to matched normal tissues. The same results were observed in colorectal cancer cell lines. Knockdown of TETs by shTET1/2/3 showed that TET family members inhibited CRC growth and metastasis. We showed that TET family member degradation by miR-506 inhibits cell proliferation and invasion in colorectal cancer.
conclusionThrough this study, we advance our understanding of the expression levels TETs and miR-506 in CRC and further clarify the internal regulatory mechanism of miR-506 by targeting TET during CRC processes. These findings may contribute to a novel avenue for researching and developing targeted therapies for CRC.
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27114802PMC4834122What OpenQuestion holds
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