Evidence map›Paper›PMID 33394291›Full record

ArticleJournal of molecular histology2021

LncRNA KCNQ1OT1 acts as miR-216b-5p sponge to promote colorectal cancer progression via up-regulating ZNF146.

Shuang Zhu, Chih-Yen Chen, Yangyang Hao

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  3. Review
  4. Article
  5. Article
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  7. Article
  8. The Roles of Zinc Finger Proteins in Colorectal Cancer.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. miR-216b-5p Inhibited the Progression of Experimental Optic Neuritis via Downregulating FAS.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  16. Review
  17. Review
  18. Article
  19. Article
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

3 authors at 3 institutions in 2 countries.

Shuang ZhuZhengZhou University, No.100 Science Ave, Gaoxin District, Zhengzhou, 450001, China.
Chih-Yen ChenCenter for General Education, National Taitung Junior College, No.911, Jhengci N. Rd, Taitung, 95045, Taiwan.
Yangyang HaoBeijing Sport University, No.48, Xinxi Road, Haidian District, Beijing, 100089, China. HYY032@163.com.ORCID http://orcid.org/0000-0003-1248-1000
Beijing Sport University · CNNational Taitung University · TWZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) have shown to act as important regulators in cancer biology. The aim of this study was to investigate the role and mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in colorectal cancer (CRC) progression. The abundance of KCNQ1OT1, microRNA-216b-5p (miR-216b-5p) and zinc finger protein 146 (ZNF146) messenger RNA (mRNA) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Cell migration and invasion abilities were assessed by transwell assays. Western blot assay was performed for determination of protein levels. LncBase v.2 of DIANA Tool and StarBase software were used to predict the targets of KCNQ1OT1 and miR-216b-5p, respectively. Dual-luciferase reporter assay was implemented to confirm the target interaction between miR-216b-5p and KCNQ1OT1 or ZNF146. KCNQ1OT1 expression was higher in CRC tissues and cell lines. KCNQ1OT1 interference restrained the proliferation, migration and invasion of CRC cells. MiR-216b-5p was a target of KCNQ1OT1 in CRC cells, and KCNQ1OT1 knockdown-induced effects in CRC cells were partly overturned by miR-216b-5p silencing. MiR-216b-5p bound to the 3' untranslated region (3'UTR) of ZNF146, and ZNF146 overexpression partly attenuated miR-216b-5p overexpression-mediated influences in CRC cells. KCNQ1OT1 up-regulated the abundance of ZNF146 through sequestering miR-216b-5p in CRC cells. KCNQ1OT1 accelerated the proliferation and motility of CRC cells through elevating ZNF146 expression via sponging miR-216b-5p. KCNQ1OT1/miR-216b-5p/ZNF146 axis might be underlying target for the diagnosis and treatment of CRC patients.

Indexed as

Disease ProgressionBase SequenceCarcinogenesisCell Line, TumorColorectal NeoplasmsGene Expression Regulation, NeoplasticGene SilencingHumansMicroRNAsPotassium Channels, Voltage-GatedUp-RegulationKCNQ1OT1 long non-coding RNA, humanMicroRNAsMIRN216 microRNA, humanPotassium Channels, Voltage-GatedColorectal cancer (CRC)KCNQ1OT1miR-216b-5pZNF146

Identifiers

PMID33394291
OpenAlexW3120976562

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.