Evidence map›Paper›PMID 30018719›Full record

ArticleAmerican journal of translational research2018

FOXK1 promotes cell growth through activating wnt/β-catenin pathway and emerges as a novel target of miR-137 in glioma.

Zhen-Gang Ji, Hai-Tao Jiang, Pei-Song Zhang

Abstract read
In one paragraph

Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

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  12. miR-137: A Novel Therapeutic Target for Human Glioma.Molecular therapy. Nucleic acids · 2020
    Review
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  17. The key genes, phosphoproteins, processes, and pathways affected by efavirenz-activated CYP46A1 in the amyloid-decreasing paradigm of efavirenz treatment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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

3 authors.

Zhen-Gang JiDepartment of Neurosurgery, Liaocheng People's Hospital Liaocheng 252000, Shandong, China.
Hai-Tao JiangDepartment of Neurosurgery, Liaocheng People's Hospital Liaocheng 252000, Shandong, China.
Pei-Song ZhangDepartment of Neurosurgery, Liaocheng People's Hospital Liaocheng 252000, Shandong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is the most common primary malignant brain tumor in adults. Forkhead box k1 (FOXK1) was reported to be dysregulated and play important roles in multiple human cancers. However, the expression pattern and roles of FOXK1 in glioma has never been investigated. In this study, we firstly observed that the expression of FOXK1 was significantly increased in glioma tissue samples and cell lines. Functional assays demonstrated that overexpression of FOXK1 promoted proliferation, cell cycle transition and inhibited apoptosis in glioma cell lines. On the contrary, knockdown of FOXK1 exhibited an opposite effect on glioma cells proliferation, cell cycle and apoptosis. Data of western blot indicated that FOXK1 overexpression increased while FOXK1 knockdown decreased the levels of β-catenin, c-myc and cyclinD1 in glioma cells. Moreover, we demonstrated that FOXK1 was a novel target of miR-137 in glioma and FOXK1 restoration abolished the tumor suppressive effect of miR-137 in glioma cells. Statistical analysis showed that the mRNA level of FOXK1 was inversely correlated with miR-137 expression in glioma tissues. In conclusion, the present study demonstrated that FOXK1 promoted cell growth through activating wnt/β-catenin pathway and is negatively regulated by miR-137 in glioma.

Indexed as

FOXK1gliomamiR-137wnt/β-catenin

Identifiers

PMID30018719
PMCPMC6038085

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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.