Evidence map›Paper›PMID 29249062›Full record

ArticleBiotechnology letters2018

Knockout of CTNNB1 by CRISPR-Cas9 technology inhibits cell proliferation through the Wnt/β-catenin signaling pathway.

Lihong Guan, Shaoyi Zhu, Yawei Han, Ciqing Yang, Yanli Liu, Liang Qiao, Xiaoying Li, Han Li, Juntang Lin

Abstract read
PubMed Publisher
In one paragraph

Article in Biotechnology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 19 citations in OpenAlex.

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  5. Biomedicines · 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

9 authors at 4 institutions in 2 countries.

Lihong Guan *College of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Shaoyi Zhu *College of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Yawei HanCollege of Food and Bioengineering, Zhengzhou University of Light Industry, Zhengzhou, China.
Ciqing YangCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Yanli LiuCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Liang QiaoCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Xiaoying LiCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Han LiCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China.
Juntang LinCollege of Life Science and Technology, Xinxiang Medical University, Xinxiang, China. linjtlin@126.com.
Xinxiang Medical University · CNUniversiti Sains Malaysia · MYXinxiang University · CNZhengzhou University of Light Industry · CN

Funding

Doctoral scientific Research Program Foundation of Xinxiang Medical University XYBSKYZZ201523Key Scientific Research Program of Higher Education in Henan Province 16A180013Key Scientific Research Program of Higher Education in Henan Province 16A180014National Natural Science Foundation of China 31000475National Natural Science Foundation of China 31440049National Natural Science Foundation of China 81600987Open Program of Henan key Laboratory of Biological psychiatry ZDSYS2015004Research Program of Foundation and Advanced Technology in Henan Province 162300410232Science and Technology Innovation Talents Program of Henan Universities 14HASTTT032
6 · The paper itself

Abstract

objectiveTo study the effects of CTNNB1 gene knockout by CRISPR-Cas9 technology on cell adhesion, proliferation, apoptosis, and Wnt/β-catenin signaling pathway.

resultsCTNNB1 gene of HEK 293T cells was knocked out by CRISPR-Cas9. This was confirmed by sequencing and western blotting. Methylthiazolyl-tetrazolium bromide assays indicated that deletion of β-catenin significantly weakened adhesion ability and inhibited proliferation rate (P < 0.01) of HEK 293T cells. Nevertheless, deletion of β-catenin did not affect apoptosis of HEK 293T cells, which was analyzed by flow cytometry with Annexin V-fluorescein isothiocyanate/propidium iodide double staining. In addition, expression level of GSK-3β, CCND1, and CCNE1 detected by qPCR and expression level of N-Cadherin and cyclin D1 detected by western blotting were significantly decreased (P < 0.01) while expression of γ-catenin detected by western blotting was significantly increased (P < 0.001).

conclusionsKnockout of CTNNB1 disturbed Wnt/β-catenin signaling pathway and significantly inhibited adhesion and proliferation of HEK 293T cells.

Indexed as

Apoptosisbeta CateninCell AdhesionCell ProliferationCRISPR-Cas SystemsGene EditingHEK293 CellsHumansWnt Signaling Pathwaybeta CateninCTNNB1 protein, humanCell adhesionCell proliferationCRISPR-Cas9CTNNB1Wnt/β-catenin signaling pathwayβ-catenin

Identifiers

PMID29249062
OpenAlexW2773198027

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.