ArticleIranian journal of pharmaceutical research : IJPR
Oncogenic Function of miR-182-5p Versus Tumor-Suppressive Activities of miR-203, miR-150-5p, and miR-139-5p via Target Gene Regulation in Colon Cancer Metastasis.
Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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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
1 citing paper in PubMed.
- Dual Targeting of CXCR4 and CXCL12 by 1,2,4-Triazole Derivatives: A Computational Approach Against Lung Cancer Metastasis.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: MicroRNAs (miRNAs) play key roles in colorectal cancer (CRC) progression and metastasis. miR-182-5p acts as an oncogenic metastamiR, frequently upregulated in cancers and promoting cell migration and invasion. In contrast, miR-203, miR-150-5p, and miR-139-5p function as tumor suppressors and are often downregulated in CRC. Methods: Expression levels of these four miRNAs were quantified in three CRC cell lines using real-time polymerase chain reaction (RT-PCR). Functional assays, including cell viability, migration, and invasion, were conducted after silencing miR-182-5p or overexpressing the tumor-suppressive miRNAs through mimic transfection. Results: The miR-182-5p was significantly overexpressed and positively correlated with metastatic potential, while miR-203, miR-150-5p, and miR-139-5p were downregulated and inversely associated with metastatic traits. Modulation of these miRNAs reduced CRC cell viability, migration, and invasion. Mechanistically, miR-182-5p enhanced metastasis via ANLN and PDE4D regulation, whereas miR-203, miR-150-5p, and miR-139-5p suppressed metastasis through PDE4D, NEGR1, and ATP11A pathways, respectively. Conclusions: These results highlight the opposing roles of miR-182-5p and the tumor-suppressive miRNAs in CRC metastasis and suggest their potential as biomarkers and therapeutic targets.
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