ArticleCell death discovery2022
Silencing circFTO inhibits malignant phenotype through modulating DUSP4 expression in clear cell renal cell carcinoma.
Article in Cell death discovery, 2022. 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 4 papers.
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.
The trial behind it
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
4 citing papers in PubMed, 6 citations in OpenAlex.
- Crosstalk between noncoding RNAs and autophagy in renal cell carcinoma: Deciphering molecular pathways and therapeutic prospects.Cancer cell international · 2025Review
- The transcription factor PITX1 cooperates with super-enhancers to regulate the expression of DUSP4 and inhibit pyroptosis in pulmonary artery smooth muscle cells.Respiratory research · 2025Article
- Hsa_circ_0014606 Derived from Exosomes Promotes Gastric Carcinoma Tumorigenesis and Proliferation by Sponging miR-514b-3p to Upregulate HNRNPC.Digestive diseases and sciences · 2024Article
- Methionine orchestrates the metabolism vulnerability in cisplatin resistant bladder cancer microenvironment.Cell death & disease · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Clear cell renal cell carcinoma (ccRCC) is the most diagnosed malignancy in kidney. Studies on the role of circular RNAs in kidney cancer are increasing. In this study, we employed high throughput sequencing and tissue micro array to detect and verify one of the key circular RNAs, circFTO, in ccRCC. The effect of circFTO on the proliferation and invasiveness of ccRCC cells and the corresponding mechanism were studied both in vitro and in vivo via multiple methods. We confirmed that circFTO was up regulated in ccRCC and correlated with a more aggressive phenotype. The up regulated circFTO could sponge and block the function of miR-514b-3p, a reported tumor suppressor, and caused overexpression of DUSP4. DUSP4 was found to lead to KRAS/ERK pathway activation, increased epithelial-mesenchymal transition (EMT) and inhibition of autophagy in ccRCC cells, which in the end boosted the proliferation and invasiveness of ccRCC. We thus concluded that circFTO/miR-514b-3p/DUSP4 axis may play an important role in ccRCC development and could be a potential biomarker and therapeutic target.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.