ArticleCancer management and research2021
LINC00261 Inhibits Esophageal Cancer Radioresistance by Down-Regulating microRNA-552-3p and Promoting DIRAS1.
Article in Cancer management and research, 2021. 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 It has been retracted, and should not be counted.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 2 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
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Functions and mechanisms of long non-coding RNA in esophageal squamous cell carcinoma (Review).Oncology letters · 2025Review
- The Mechanism of Long Non-coding RNA in Cancer Radioresistance/Radiosensitivity: A Systematic Review.Frontiers in pharmacology · 2022Review
Corrections and comments
- Retraction · 2023-11-11Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Paper Mill · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/689DAB6588976C622E2F75A4C3608C
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEsophageal cancer (EC) represents a life-threatening tumor with an ever-increasing incidence rate. Long intergenic non-protein coding RNAs (LINCs) have also become a topic of interest in EC. In a similar light, the current study aimed to investigate the role of LINC00261 in EC radioresistance.
methodsFirstly, radioresistant EC cell lines TE-1-R and TE-5-R were established using TE-1 and TE-5 cells. Subsequently, LINC00261, microRNA (miR)-552-3p, and DIRAS1 expression patterns in EC tissues and adjacent normal tissues and EC cells were evaluated. In addition, survival fraction (SF), colony formation, apoptosis, and γ-H2AX levels were analyzed, followed by the detection of the binding relation between LINC00261 and miR-552-3p and between miR-552-3p and DIRAS1. Lastly, xenograft transplantation was carried out to confirm the effects of LINC00261 on EC radioresistance in vivo.
resultsLINC00261 and DIRAS1 were poorly-expressed in EC tissues and cells, but miR-552-3p was over-expressed. In EC cells with X-ray radiation, over-expression of LINC00261 reduced SF and cell viability, strengthened γ-H2AX levels, and promoted apoptosis, while all these trends were counteracted by miR-522-3p over-expression or DIRAS1 silencing. Mechanistic investigation further validated the binding relation between LINC00261 and miR-552-3p, and between miR-552-3p and DIRAS1. Moreover, LINC00261 over-expression suppressed tumor growth and reduced EC radioresistance in vivo.
conclusionAltogether, our findings indicated that LINC00261 exerts a suppressive effect on EC radioresistance via the competing endogenous RNA network to sponge miR-552-3p and up-regulate DIRAS1 transcription.
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