ArticleExperimental and therapeutic medicine2020
miR-25 expression is upregulated in pancreatic ductal adenocarcinoma and promotes cell proliferation by targeting ABI2.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed, 8 citations in OpenAlex.
- Role of exosomal noncoding RNA in esophageal carcinoma.Frontiers in oncology · 2023Review
- Abi1 mediates airway smooth muscle cell proliferation and airway remodeling via Jak2/STAT3 signaling.iScience · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are reported to play a critical role in the regulation of cancer cell proliferation; however, the role of microRNA-25 (miR-25) in pancreatic ductal adenocarcinoma (PDAC) remains unclear. In the present study, the role of miR-25 in PDAC cell proliferation was investigated. Upregulated expression of miR-25 was found in PDAC tissues and cell lines by reverse transcription-quantitative PCR. Cell proliferation was significantly enhanced by overexpression of miR-25 as shown by CCK-8 assay results. Meanwhile, overexpression of miR-25 also promoted G1-to-S phase transition of the cell cycle in Aspc-1 cells via flow cytometry analysis. However downregulation of miR-25 inhibited the tumor cell proliferation and cell cycle transition. Online software was used to predict the target gene for miR-25 and luciferase reporter assay confirmed that Abl interactor 2 (
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