Evidence map›Paper›PMID 31702026›Full record

ArticleMolecular medicine reports2019

Knockdown of long noncoding RNA DLEU1 suppresses the progression of renal cell carcinoma by downregulating the Akt pathway.

Genquan Yue, Caixia Chen, Ligang Bai, Guoqiang Wang, Yong Huang, Yunbin Wang, Hongwei Cui, Yunfeng Xiao

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 36% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 12 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Genquan YueDepartment of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China.
Caixia ChenClinical Medical Research Center, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China.
Ligang BaiDepartment of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China.
Guoqiang WangDepartment of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China.
Yong HuangDepartment of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China.
Yunbin WangDepartment of Urology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China.
Hongwei CuiClinical Medical Research Center, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010000, P.R. China.
Yunfeng XiaoThe Center for New Drug Safety Evaluation and Research of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010110, P.R. China.
Inner Mongolia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are involved in the tumorigenesis and progression of various types of cancer. The lncRNA deleted in lymphocytic leukemia 1 (DLEU1) has been reported to be dysregulated in cancer cells and thus associated with tumor development; however, the role of DLEU1 in renal cell carcinoma (RCC) remains unclear. In the present study, DLEU1 was knocked down using small interfering RNA in the RCC cell lines KETR3 and 786‑O to determine the role of DLEU1. Cell Counting Kit‑8, colony formation, Transwell and flow cytometry assays were performed to assess the effects of DLEU1 on cell proliferation, migration, invasion and apoptosis in KETR3 and 786‑O cells. The protein expression levels of factors associated with apoptosis and epithelial‑mesenchymal transition (EMT) were examined by western blot. The results demonstrated that silencing DLEU1 decreased the growth capacity, migration and invasion of KETR3 and 786‑O cells. Additionally, loss of DLEU1 was observed to stimulate the mitochondrial pathway of cell apoptosis via regulation of the expression of Bcl‑2/Bax, cleaved caspase‑3 and cleaved caspase‑9 in KETR3 and 786‑O cells. Furthermore, DLEU1 knockdown significantly inhibited the protein kinase B (Akt) pathway by downregulating the expression of phosphorylated‑Akt, cyclin  D1 and P70S6 kinase. In addition, depletion of DLEU1 was observed to impair the process of EMT in RCC cells via the upregulation of E‑cadherin, and downregulation of N‑cadherin and vimentin. Collectively, these results indicated a pro‑oncogenic role of DLEU1 in the progression and development of RCC via modulation of the Akt pathway and EMT phenotype.

Indexed as

Down-RegulationGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticSignal TransductionCarcinoma, Renal CellCell Line, TumorGene Knockdown TechniquesHumansKidney NeoplasmsProto-Oncogene Proteins c-aktRNA, Long NoncodingRNA, NeoplasmProto-Oncogene Proteins c-aktRNA, Long NoncodingRNA, Neoplasm

Identifiers

PMID31702026
PMCPMC6797951
OpenAlexW2975631698

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Registered trials

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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.