Evidence map›Paper›PMID 34709960›Full record

ArticleTechnology in cancer research & treatment

CBX2 Induces Glioma Cell Proliferation and Invasion Through the Akt/PI3K Pathway.

Le Wang, Bingcheng Ren, Hao Zhuang, Yue Zhong, Yang Nan

Open access · goldAbstract read
In one paragraph

Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Le Wang117865Tianjin Medical University General Hospital, Tianjin, China.ORCID 0000-0003-2475-5312
Bingcheng Ren117865Tianjin Medical University General Hospital, Tianjin, China.
Hao ZhuangCancer Hospital Affiliated to Zhengzhou University, Zhengzhou, Henan, China.
Yue Zhong117865Tianjin Medical University General Hospital, Tianjin, China.
Yang Nan117865Tianjin Medical University General Hospital, Tianjin, China.
Tianjin Medical University General Hospital · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is the most common primary intracranial tumor. Abnormal expression of CBX2 (ChromoBox2) is associated with tumorigenesis and tumor development. TCGA data in UALCAN showed that CBX2 was overexpressed in glioma tissue. To confirm the role of CBX2 in glioma, we regulated the level of CBX2 and conducted colony formation, Transwell, and CCK-8 assays to verify the effect of CBX2. The results showed that CBX2 knockdown reduced glioma cell proliferation and invasion and that the cells were less tumorigenic. CBX2 overexpression induced glioma cell proliferation and invasion and glioma stem cell self-renewal. The animal experiments showed that CBX2 knockdown inhibited glioma growth and improved survival time. CBX2 knockdown inhibited activation of the Akt/PI3K pathway. epidermal growth factor rescued the effects of CBX2. CBX2 could induce the growth and invasion of glioma cells via the Akt/PI3K pathway.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorBrain NeoplasmsCase-Control StudiesCell ProliferationCell Self RenewalGliomaHumansMaleMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessPhosphatidylinositol 3-KinasesBiomarkers, TumorCBX2 protein, humanPhosphatidylinositol 3-KinasesPolycomb Repressive Complex 1Proto-Oncogene Proteins c-aktAktCBX2gliomaPI3K

Identifiers

PMID34709960
PMCPMC8558802
OpenAlexW3131086150

What OpenQuestion holds

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LicenceCC BY-NC
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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.