ArticleTranslational cancer research2020
LncRNA FAM66C inhibits pancreatic cancer progression by sponging miR-574-3p.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- A novel cuproptosis-associated LncRNA model predicting prognostic and immunotherapy response for glioma.Discover oncology · 2025Article
- LncRNA FAM66C predicts poor prognosis in patients with lung adenocarcinoma and regulates cell proliferation and metastasis via miR-339-3p.Journal of cardiothoracic surgery · 2025Article
- Article
- Erratum to lncRNA FAM66C inhibits pancreatic cancer progression by sponging miR-574-3p.Translational cancer research · 2024Article
- A novel neutrophil extracellular traps-related lncRNA signature predicts prognosis in patients with early-stage lung adenocarcinoma.Annals of medicine · 2023Article
- LncRNA-FAM66C Was Identified as a Key Regulator for Modulating Tumor Microenvironment and Hypoxia-Related Pathways in Glioblastoma.Frontiers in public health · 2022Article
- LINC00857 promotes the proliferation of pancreatic cancer via MET, STAT3, and CREB.Journal of gastrointestinal oncology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPancreatic cancer is an extensively concerned human malignancy around the globe, yet the potential therapeutic target remains to be further determined. MicroRNA and LncRNA have been reported to be involved in progression of pancreatic cancer, while the biological role of microRNA-574-3p (miR-574-3p) and FAM66C in pancreatic cancer development is poorly investigated.
methodsQuantitative real-time PCR (qPCR) analysis was employed to detect the expression of miR-574-3p and FAM66C in pancreatic normal or cancerous tissues and cells. The proliferative and apoptosis signaling molecules were also examined via qPCR and western blot separately. Additionally, cell proliferation and apoptosis assay were performed via CCK8, colony formation and Annexin V-FITC apoptosis assay. Interaction between miR-574-3p and FAM66C was interrogated by luciferase reporter assay and RNA immunoprecipitation. Even more, a pancreatic cancer xenograft mice assay was implemented to illustrate the coordinating role of miR-574-3p and FAM66C in pancreatic cancer proliferation.
resultsWe found that levels of miR-574-3p were significantly higher in cancer tissues and cells compared to normal (P<0.05). Remarkably, the results indicated that depletion of miR-574-3p inhibited proliferation and promoted apoptosis of human pancreatic cancer cell lines. Additionally, FAM66C was demonstrated to interact with miR-574-3p and inhibit its expression. Significantly, FAM66C was proved to act as a tumor suppressor role via inhibiting cell proliferation and promoting cell apoptosis in pancreatic cancer. Moreover, FAM66C coordinated with miR-574-3p to regulate progression of xenograft tumor in the nude mice.
conclusionsFAM66C-miR-574-3p axis mediates progression of pancreatic and might be the promising therapeutic target for pancreatic cancer patients.
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