ArticleOncoTargets and therapy2020
LINC00565 Enhances Proliferative Ability in Endometrial Carcinoma by Downregulating KLF9.
Article in OncoTargets and therapy, 2020. 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 It has been retracted, and should not be counted.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 3 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- The Impact of High lncRNA Expression on Clinicopathological Characteristics and Prognosis of Endometrial Cancer Patients: A Meta-Analysis.Cancer medicine · 2025Pooled it
- β-Sitosterol Inhibits The Proliferation of Endometrial Cells via Regulating Smad7-Mediated TGF-β/Smads Signaling Pathway.Cell journal · 2023Article
- Article
Corrections and comments
- Retraction · 2023-05-15Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/A50ADAF95A2F57037C70CAB315FC11
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo detect LINC00565 expression level in endometrial carcinoma (EC) samples and cell lines, and the correlations between LINC00565 and clinical features of EC patients. After intervening LINC00565, the underlying mechanism about proliferative ability in EC cell lines is observed.
methodsRelative levels of LINC00565 and KLF9 in 52 paired EC and paracancerous tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between relative level of LINC00565 or KLF9 and clinical features of EC patients was analyzed. After knockdown of LINC00565 and KLF9, potential regulations of them on biological functions of EC were examined by Cell Counting Kit (CCK-8), colony formation assay and in vivo xenograft model in nude mice, respectively. At last, dual-luciferase reporter assay and rescue experiments were conducted to illustrate the mechanisms of LINC00565 and KLF9 in mediating the development of EC.
resultsLINC00565 was upregulated in EC tissues. Chi-square analysis showed that a high level of LINC00565 predicted large tumor size, advanced pathological staging and poor prognosis in EC. Silence of LINC00565 decreased proliferative ability in EC cells and tumor growth in nude mice bearing EC. KLF9 was the target gene of LINC00565. The negative interaction between LINC00565 and KLF9 was responsible for stimulating the malignant development of EC. Knockdown of KLF9 could abolish the regulatory effects of silenced LINC00565 on proliferative ability and tumorigenesis in EC.
conclusionLINC00565 is upregulated in EC tissues and closely linked to tumor size, pathological staging and poor prognosis in EC patients. LINC00565 stimulates proliferative ability in EC by downregulating KLF9.
Indexed as
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.