Evidence map›Paper›PMID 33824420›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2021

LncRNA UCC promotes epithelial-mesenchymal transition via the miR-143-3p/SOX5 axis in non-small-cell lung cancer.

Ri Chen, Chunfan Zhang, Yuanda Cheng, Shaoqiang Wang, Hang Lin, Heng Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  15. The role of PI3K/AKT signaling pathway in gallbladder carcinoma.American journal of translational research · 2022
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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 3 institutions in 1 country.

Ri ChenDepartment of Cardiothoracic Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, PR China.
Chunfan ZhangDepartment of General Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, PR China.
Yuanda ChengDepartment of General Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, PR China.
Shaoqiang WangDepartment of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, JiNing, Shandong, PR China.
Hang LinDepartment of General Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, PR China.
Heng ZhangDepartment of General Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, PR China. zhmm078@163.com.
Central South University · CNXiangya Hospital Central South University · CNAffiliated Hospital of Jining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) have been found to play regulatory roles in cancers; for example, UCC was reported to promote colorectal cancer progression. However, the function of UCC in non-small-cell lung cancer (NSCLC) remains unclear. Therefore, mRNA and protein levels were assessed using qPCR and western blots. Cell viability was assessed by colony-formation assays. The interaction between lncRNAs and miRNAs was detected by dual-luciferase reporter and RIP assays. The tumorigenesis of NSCLC cells in vivo was determined by xenograft assays. LncRNA UCC was highly expressed in both NSCLC tissues and cells. Knockdown of UCC expression suppressed the proliferation of NSCLC cells. In addition, a dual-luciferase reporter system and RIP assays showed that UCC specifically bound to miR-143-3p and acted as a sponge of miR-143-3p in NSCLC cells. The miR-143-3p inhibitor rescued the inhibitory effect of sh-UCC on the proliferation of NSCLC cells. Moreover, miR-143-3p and UCC showed opposite effects on the expression of SOX5, which promoted EMT in NSCLC cells. In addition, in a mouse model, knockdown of UCC expression alleviated EMT and NSCLC progression in vivo, which was consistent with the in vitro results. In the current study, we found that UCC induced the proliferation and migration of NSCLC cells both in vitro and in vivo by inducing the expression of SOX5 via miR-143-3p and subsequently promoted EMT in NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMicroRNAsRNA, Long NoncodingA549 CellsAnimalsEpithelial-Mesenchymal TransitionHeterograftsHumansMaleMiceMice, Inbred BALB CMice, NudeSOXD Transcription FactorsMicroRNAsMIRN143 microRNA, humanRNA, Long NoncodingSOX5 protein, humanSOXD Transcription Factors

Identifiers

PMID33824420
OpenAlexW3140383199

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.