ArticleExperimental and therapeutic medicine2020
MicroRNA-23a acts as an oncogene in pancreatic carcinoma by targeting TFPI-2.
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 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Venous Thrombogenesis and Cervical Cancer: Plasma MicroRNAs as Prognostic Indicators of Tumor Behavior.International journal of molecular sciences · 2025Article
- Reassessing the Role of Tissue Factor Pathway Inhibitor 2 in Neoplastic and Non-Neoplastic Lesions.Cancers · 2025Review
- Plasma microRNA Environment Linked to Tissue Factor Pathway and Cancer-Associated Thrombosis: Prognostic Significance in Ovarian Cancer.Biomolecules · 2024Article
- Functional and Potential Therapeutic Implication of MicroRNAs in Pancreatic Cancer.International journal of molecular sciences · 2023Review
- AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression.Discover oncology · 2023Article
- Mechanism of HBx carcinogenesis interaction with non-coding RNA in hepatocellular carcinoma.Frontiers in oncology · 2023Review
- mEpigenetics · 2022Article
- Insights Into the Biological Role of NEDD4L E3 Ubiquitin Ligase in Human Cancers.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic carcinoma (PC) is a rapidly progressive, fatal malignant tumor with the poorest prognosis among all major carcinoma types. MicroRNAs (miRNAs/miRs) have been indicated to be key post-transcriptional regulatory factors, which are involved in cancer development. The present study was designed to investigate the effect of miR-23a on PC cell proliferation, metastasis and apoptosis. The expression of miR-23a was detected in a normal pancreatic ductal epithelial cell line and three PC cell lines, and miR-23a inhibitor or mimics were transfected into the Panc-1 and MiaPaCa2 PC cells. The association between miR-23a and tissue factor pathway inhibitor (TFPI)-2 was examined using a luciferase reporter assay. MTT and flow cytometry assays were used to assess cell viability and apoptosis, respectively. Furthermore, wound-healing, Transwell and Matrigel assays were used to evaluate cell migration and invasion abilities, and the protein expression level of TFPI-2 was determined using western blot analysis. The results of the present study revealed that miR-23a was upregulated in PC cells. Furthermore, TFPI-2 was identified as a downstream target of miR-23a, and TFPI-2 expression was found to be increased following miR-23a knockdown. In addition, functional assays revealed that downregulation of miR-23a decreased PC cell proliferation, migration and invasiveness and promoted cell apoptosis, while miR-23a overexpression exerted the opposite effects. Furthermore, TFPI-2 knockdown rescued the biological effects on PC cells, which were induced by miR-23a knockdown. The results of the present study indicated that miR-23a negatively modulated TFPI-2 expression
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