Evidence map›Paper›PMID 33097685›Full record

ArticleCell death & disease2020

The long noncoding RNA LUCAT1 promotes colorectal cancer cell proliferation by antagonizing Nucleolin to regulate MYC expression.

Runliu Wu, Liang Li, Yang Bai, Bowen Yu, Canbin Xie, Hao Wu, Yi Zhang, Lihua Huang, Yichao Yan, Xiaorong Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 65 citations in OpenAlex.

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  10. The MYC/TXNIP axis mediates NCL-Suppressed CD8Molecular medicine (Cambridge, Mass.) · 2025
    Article
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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

11 authors at 3 institutions in 1 country.

Runliu WuDepartment of Gastrointestinal surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China.
Liang LiClass 25 grade 2016, The Five-Year Program in Clinical Medicine, School of Medicine, University of South China, Hengyang, Hunan, 421001, China.
Yang BaiDepartment of Gastrointestinal surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China.
Bowen YuDepartment of Gastrointestinal surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China.
Canbin XieDepartment of Gastrointestinal surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China.
Hao WuDepartment of Gastrointestinal surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China.
Yi ZhangDepartment of Gastrointestinal surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China.
Lihua HuangCenter for Experimental Medicine, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China.
Yichao YanDepartment of Gastroenterological Surgery, Peking University International Hospital, Beijing, 102206, China.
Xiaorong LiDepartment of Gastrointestinal surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China. xiaorongli@csu.edu.cn.
Changwei LinDepartment of Gastrointestinal surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China. linchangwei1987@csu.edu.cn.
Central South University · CNPeking University International Hospital · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The long noncoding RNA (lncRNA) LUCAT1 was recently reported to be upregulated and to play an essential role in multiple cancer types, especially colorectal cancer (CRC), but the molecular mechanisms of LUCAT1 in CRC are mostly unreported. Here, a systematic analysis of LUACT1 expression is performed with data from TCGA database and clinic CRC samples. LUCAT1 is identified as a putative oncogene, which is significantly upregulated in CRC and is associated with poor prognosis. Loss of LUCAT1 restricts CRC proliferative capacities in vitro and in vivo. Mechanically, NCL is identified as the protein binding partner of LUCAT1 by using chromatin isolation by RNA purification coupled with mass spectrometry (ChIRP-MS) and RNA immunoprecipitation assays. We also show that NCL directly binds to LUCAT1 via its putative G-quadruplex-forming regions from nucleotides 717 to 746. The interaction between LUCAT1 and NCL interferes NCL-mediated inhibition of MYC and promote the expression of MYC. Cells lacking LUCAT1 show a decreased MYC expression, and NCL knockdown rescue LUCAT1 depletion-induced inhibition of CRC cell proliferation and MYC expression. Our results suggest that LUCAT1 plays a critical role in CRC cell proliferation by inhibiting the function of NCL via its G-quadruplex structure and may serve as a new prognostic biomarker and effective therapeutic target for CRC.

Indexed as

AnimalsCell Line, TumorCell ProliferationColorectal NeoplasmsFemaleGenes, mycHeterograftsHumansMaleMiceMice, Inbred BALB CMice, NudeMiddle AgedNucleolinPhosphoproteinsPrognosislong non-coding RNA LUCAT1, humanMYC protein, humanNucleolinPhosphoproteinsProto-Oncogene Proteins c-mycRNA-Binding ProteinsRNA, Long Noncoding

Identifiers

PMID33097685
PMCPMC7584667
OpenAlexW3093923210

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.