ArticleBioMed research international2023
Long Noncoding RNA LINC01503 Silencing Suppresses KLK4 Expression to Impede Pancreatic Cancer Development as miR-1321 Sponge.
Article in BioMed research international, 2023. 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 It has been retracted, and should not be counted.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
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
2 citing papers in PubMed, 1 citations in OpenAlex.
- [Isoliquiritigenin Modulates the Effect of LINC01503 on Lung Squamous Carcinoma Cells].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Article
- Retracted: Long Noncoding RNA LINC01503 Silencing Suppresses KLK4 Expression to Impede Pancreatic Cancer Development as miR-1321 Sponge.BioMed research international · 2023Article
Corrections and comments
- Retraction · 2023-08-02Concerns/Issues about Data · Concerns/Issues about Referencing/Attributions · Concerns/Issues about Peer Review · Investigation by Journal/Publisher · Investigation by Third Party · Unreliable Results and/or Conclusions · · See also: https://pubpeer.com/publications/0A85D252C734647B454187F9285429
- Retracted
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Long intergenic nonprotein coding RNA 1503 (LINC01503) was reportedly oncogenic in several malignancies, whereas whether it contributed to pancreatic cancer tumorigenesis and progression requires to be verified. Methods: The expression pattern of LINC01503 was monitored via qRT-PCR assay in normal cells and cancerous pancreatic cancer cells. The introduction of silencing LINC01503 was to verify the relation between LINC01503 expression and cell growth. Then, the targeting relationship of LINC01503 to miR-1321 was confirmed by bioinformatics predication and luciferase reporter assay. In addition, luciferase reporter assays evaluated the binding of miR-1321 to the 3'-untranslated region of KLK4. Overexpressing KLK4 and inhibiting LINC01503 was introduced in tumor cells to investigate the corresponding impacts on pancreatic cancer cell proliferation and migration. Results: LINC01503 and KLK4 were highly abundant in pancreatic cancer cells. Mechanistically, miR-1321 bound to LINC01503 and KLK4. Downregulating LINC01503 promoted the availability of miR-1321 in pancreatic cancer cells and thus repressed KLK4 expression. KLK4 overexpression abolished the impediment of LINC01503 depletion on cell proliferation and migration. Conclusion: Oncogenic function of LINC01503 was dependent on KLK4 upregulation by sponging miR-1321. Revealing the tumor-promoting property of LINC01503 in pancreatic cancer may confer new biomarkers for this malignancy.
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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.