Evidence map›Paper›PMID 31592114›Full record

ArticleCell & bioscience2019

Long noncoding RNA lnc-DILC stabilizes PTEN and suppresses clear cell renal cell carcinoma progression.

Han Zhang, Pengtao Wei, Wenwei Lv, Xingtao Han, Jinhui Yang, Shuaifeng Qin

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. LncRNA AC098613.1 promotes acute myeloid leukemia cell differentiation through CDC5L/ADAP1/NRD1 axis.Apoptosis : an international journal on programmed cell death · 2026
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  6. Cancer resistance via the downregulation of the tumor suppressorsExploration of targeted anti-tumor therapy · 2023
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  12. Long Non-CodingNon-coding RNA · 2021
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  19. Long Non-coding RNAFrontiers in oncology · 2020
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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

6 authors at 1 institution in 1 country.

Han ZhangUrology Department, Luoyang Central Hospital, No. 288, Zhongzhou Road, Luoyang, 471000 Henan China.ORCID 0000-0003-4174-7736
Pengtao WeiUrology Department, Luoyang Central Hospital, No. 288, Zhongzhou Road, Luoyang, 471000 Henan China.
Wenwei LvUrology Department, Luoyang Central Hospital, No. 288, Zhongzhou Road, Luoyang, 471000 Henan China.
Xingtao HanUrology Department, Luoyang Central Hospital, No. 288, Zhongzhou Road, Luoyang, 471000 Henan China.
Jinhui YangUrology Department, Luoyang Central Hospital, No. 288, Zhongzhou Road, Luoyang, 471000 Henan China.
Shuaifeng QinUrology Department, Luoyang Central Hospital, No. 288, Zhongzhou Road, Luoyang, 471000 Henan China.
Luoyang Central Hospital Affiliated to Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence has indicated that long noncoding RNAs (lncRNAs) are crucial regulators affecting the progression of human cancers. Recently, lncRNA downregulated in liver cancer stem cells (lnc-DILC) was identified to function as a tumor suppressor inhibiting the tumorigenesis and metastasis in liver cancer and colorectal cancer. However, to date, little is known about the functional roles of lnc-DILC in modulating malignant phenotypes of clear cell renal cell carcinoma (ccRCC) cells.

methodslnc-DILC expression in human ccRCC tissues was detected by qRT-PCR. Overexpression and knockdown experiments were carried out to determine the effects of lnc-DILC on ccRCC cell proliferation, migration and invasion. To reveal the underlying mechanisms of lnc-DILC functions in ccRCC cells. RNA immunoprecipitation, RNA pull-down, in vivo ubiquitination, co-immunoprecipitation and western blot assays were performed.

resultsHere, we identified that lnc-DILC levels were dramatically downregulated in ccRCC tissues. Loss of lnc-DILC expression was correlated with larger tumor size, advanced tumor grade and lymph node metastasis, and also predicted worse prognosis in patients with ccRCC. Functionally, knockdown and overexpression experiments demonstrated that lnc-DILC inhibited cell proliferation, migration and invasion in ccRCC cells. Mechanistic investigation revealed that lnc-DILC bound to tumor suppressor PTEN and suppressed its degradation. lnc-DILC repressed the PTEN ubiquitination through blocking the interaction between PTEN and E3 ubiquitin ligase WWP2 and recruiting the deubiquitinase USP11 to PTEN. Moreover, we demonstrated that PTEN-AKT signaling was crucial for lnc-DILC-mediated suppressive effects.

conclusionsIn summary, our research revealed a novel mechanism by which lnc-DILC regulates PTEN stability via WWP2 and USP11, and shed light on potential therapeutic strategies by the restoration of lnc-DILC expression in patients with ccRCC.

Indexed as

PTENUbiquitinationUSP11WWP2

Identifiers

PMID31592114
PMCPMC6775667
OpenAlexW2979140709

What OpenQuestion holds

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LicenceCC BY
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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.