ArticleDiscover oncology2022
Silencing of long non-coding RNA TUC338 inhibits the malignant phenotype of nasopharyngeal cancer cells via modulating the miR-1226-3p/FGF2 axis.
Article in Discover oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 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.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- MIR210HG Accelerates the Progression of Colorectal Cancer and Affects the Function of Colorectal Cancer Cells by Downregulating miR-1226-3p.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024Article
- Epigenetic priming of an epithelial enhancer by p63 and CTCF controls expression of a skin-restricted gene XP33.Cell death discovery · 2023Article
- Involvement of transcribed lncRNA uc.291 in hyperproliferative skin disorders.Biology direct · 2023Article
- p63: a crucial player in epithelial stemness regulation.Oncogene · 2023Review
- Article
Corrections and comments
- Retraction · 2024-10-23Error in Methods · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs (lncRNAs) have been suggested as essential regulators in the cancer progression. LncRNA TUC338 was found to promote the malignancy of various cancers, however, the involvement of TUC338 in nasopharyngeal cancer (NPC) has not been well characterized. Here, our results found the significant overexpression of TUC338 in NPC tissues. Higher level of TUC338 was also observed in NPC cells. Interestingly, NPC patients harboring overexpressed TUC338 have worse prognosis. Functional study indicated that down-regulated TUC338 remarkably suppressed the NPC cell proliferation and cell migration. Notably, depletion of TUC338 significantly inhibited the in vivo tumor growth. Mechanistically, TUC338 acted as molecular sponge of miR-1226-3p and attenuated the negative regulation of miR-1226-3p on the expression of fibroblast growth factor 2 (FGF2). Down-regulation of TUC338 inhibited FGF2 expression in NPC cells and tumor tissues. Overexpression of FGF2 attenuated the suppressed NPC proliferation upon the depletion of TUC338. Our results demonstrated the novel function of TUC338/miR-1226-3p/FGF2 axis in NPC progression, suggesting the potential diagnosis and therapeutics significance of TUC338 in NPC.
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