Evidence map›Paper›PMID 33682985›Full record

ArticleThe journal of gene medicine2021

Long non-coding RNA KCNQ1OT1 promotes the progression of gastric cancer via the miR-145-5p/ARF6 axis.

Xiongdong Zhong, Xiaoyan Wen, Lei Chen, Ni Gu, Xianchang Yu, Kang Sui

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The journal of gene medicine, 2021. 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 It has been retracted, and should not be counted.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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. World journal of gastrointestinal oncology · 2024
    Article
  2. CircZNF236 facilitates malignant progression in oral squamous cell carcinoma by sequestering miR-145-5p.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Xiongdong ZhongDepartment of Cardiothoracic Surgery, Zhuhai People's Hospital (Zhuhai hospital affiliated with Jinan University), Zhuhai City, Guangdong Province, China.
Xiaoyan WenDepartment of Cardiothoracic Surgery, Zhuhai People's Hospital (Zhuhai hospital affiliated with Jinan University), Zhuhai City, Guangdong Province, China.
Lei ChenDepartment of Cardiothoracic Surgery, Zhuhai People's Hospital (Zhuhai hospital affiliated with Jinan University), Zhuhai City, Guangdong Province, China.
Ni GuDepartment of Cardiothoracic Surgery, Zhuhai People's Hospital (Zhuhai hospital affiliated with Jinan University), Zhuhai City, Guangdong Province, China.
Xianchang YuDepartment of Cardiothoracic Surgery, Zhuhai People's Hospital (Zhuhai hospital affiliated with Jinan University), Zhuhai City, Guangdong Province, China.
Kang SuiDepartment of Cardiothoracic Surgery, Zhuhai People's Hospital (Zhuhai hospital affiliated with Jinan University), Zhuhai City, Guangdong Province, China.ORCID 0000-0003-4529-8739
Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding RNA KCNQ1 opposite strand/antisense transcript one gene (KCNQ1OT1) has been reported to be involved in the progression of many types of human cancer, whereas its role in gastric cancer (GC) remains unknown. The present study aimed to investigate the role of KCNQ1OT1 in GC.

methodsIn total, 25 GC tissues and adjacent normal tissues were collected. The expression of KCNQ1OT1, miR-145-5p and ARF6 in GC tissues and cell lines was detected by quantitative reverse transcriptase-polymerase chain reaction or western blotting. Bioinformatics analysis and a dual luciferase reporter assay were performed to determine the relationship between KCNQ1OT1 and miR-145-5p or miR-145-5p and ARF6. Gain- and loss-of function of KCNQ1OT1 and miR-145-5p were achieved to confirm their roles in GC cells. Cell counting kit-8, colony formation and flow cytometry assays were used to evaluate cell viability, proliferation and apoptosis. A xenograft tumor model was established with BGC803 tumor cells transfected with sh-KCNQ1OT1 or empty vector to determine the role of LINC01089 in vivo.

resultsThe expression levels of KCNQ1OT1 were markedly elevated in GC tissues and cells. Knockdown of KCNQ1OT1 inhibited GC tumor growth, reduced GC cell viability and colony formation, and induced GC cell apoptosis. The expression levels of miR-145-5p were significantly decreased in GC cells and correlated with the expression of KCNQ1OT1 in GC tumors. Moreover, KCNQ1OT1 directly binds with miR-145-5p, which is targeting ARF6. Knockdown of KCNQ1OT1 increased the expression levels of miR-145-5p. Inhibition of miR-145-5p increased the expression levels of KCNQ1OT1 and also attenuated the effects of knockdown of KCNQ1OT1 on the viability, proliferation and apoptosis of GC cells. In addition, overexpression of miR-145-5p reduced GC cell viability and colony formation and induced GC cell apoptosis, whereas overexpression of ARF6 attenuated the effects of overexpression of miR-145-5p on GC cell viability, colony formation and apoptosis.

conclusionsKCNQ1OT1 can promote GC progression through the miR-145-5p/ARF6 axis. KCNQ1OT1 may serve as a therapeutic target and a diagnostic biomarker of GC.

Indexed as

ADP-Ribosylation Factor 6AgedApoptosisCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMaleMicroRNAsMiddle AgedPotassium Channels, Voltage-GatedSignal TransductionStomach NeoplasmsADP-Ribosylation Factor 6ARF6 protein, humanKCNQ1OT1 long non-coding RNA, humanMicroRNAsMIRN145 microRNA, humanPotassium Channels, Voltage-GatedARF6gastric cancerKCNQ1OT1miR-145-5p

Identifiers

PMID33682985
PMCPMC8244094
OpenAlexW3134967293

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.