ArticleHereditas2026
miR-1229-3p promotes epithelial-mesenchymal transition and metastasis of cervical cancer cells by targeting FBXL5.
Article in Hereditas, 2026. 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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Who cites it
1 citing paper in PubMed.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to explore the biological function of miR-1229-3p in the occurrence and development of cervical cancer (CC).
methodsThe expression levels of miR-1229-3p and FBXL5 in CC tissues and cell lines were detected by RT-qPCR. Cell proliferation ability was evaluated by MTT. Cell migration and invasion abilities were detected by Transwell. The expression of EMT-related markers were detected by RT-qPCR. The targeting relationship between miR-1229-3p and FBXL5 was verified by dual luciferase reporter assay.
resultsThe expression of miR-1229-3p was significantly upregulated in CC tissues and CC cell lines. High expression of miR-1229-3p was associated with poor differentiation and lymph node metastasis. Overexpression of miR-1229-3p could promote the proliferation, migration, invasion of CC cells, and induce the EMT process. Dual luciferase reporter assays confirmed that FBXL5 was the direct target gene of miR-1229-3p, and their expressions showed a significant negative correlation in CC tissues. Overexpression of FBXL5 could reverse the carcinogenic effects caused by miR-1229-3p.
conclusionmiR-1229-3p directly inhibits the expression of FBXL5, thereby activating the EMT process, and ultimately promoting the proliferation, migration, and invasion of CC cells.
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