Evidence map›Paper›PMID 28620820›Full record

ArticleMolecular and cellular biochemistry2018

Cytoglobin inhibits migration through PI3K/AKT/mTOR pathway in fibroblast cells.

Selami Demirci, Ayşegül Doğan, Hüseyin Apdik, Emre Can Tuysuz, Sukru Gulluoglu, Omer Faruk Bayrak, Fikrettin Şahin

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 23 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

7 authors at 2 institutions in 2 countries.

Selami DemirciDepartment of Genetics and Bioengineering, Faculty of Engineering and Architecture, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey.
Ayşegül DoğanDepartment of Genetics and Bioengineering, Faculty of Engineering and Architecture, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey. aysegul.dogan@nih.gov.
Hüseyin ApdikDepartment of Genetics and Bioengineering, Faculty of Engineering and Architecture, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey.
Emre Can TuysuzDepartment of Genetics and Bioengineering, Faculty of Engineering and Architecture, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey.
Sukru GulluogluDepartment of Genetics and Bioengineering, Faculty of Engineering and Architecture, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey.
Omer Faruk BayrakDepartment of Medical Genetics, Yeditepe University Medical School Inonu Mah, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey.
Fikrettin ŞahinDepartment of Genetics and Bioengineering, Faculty of Engineering and Architecture, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755, Atasehir, Istanbul, Turkey.
Yeditepe University · TRNational Heart Lung and Blood Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell proliferation and migration are crucial in many physiological processes including development, cancer, tissue repair, and wound healing. Cell migration is regulated by several signaling molecules. Identification of genes related to cell migration is required to understand molecular mechanism of non-healing chronic wounds which is a major concern in clinics. In the current study, the role of cytoglobin (CYGB) gene in fıbroblast cell migration and proliferation was described. L929 mouse fibroblast cells were transduced with lentiviral particles for CYGB and GFP, and analyzed for cell proliferation and migration ability. Fibroblast cells overexpressing CYGB displayed decreased cell proliferation, colony formation capacity, and cell migration. Phosphorylation levels of mTOR and two downstream effectors S6 and 4E-BP1 which take part in PI3K/AKT/mTOR signaling declined in CYGB-overexpressing cells. Microarray analysis indicated that CYGB overexpression leads to downregulation of cell proliferation, migration, and tumor growth associated genes in L929 cell line. This study demonstrated the role of CYGB in fibroblast cell motility and proliferation. CYGB could be a promising candidate for further studies as a potential target for diseases related to cell migration such as cancer and chronic wound treatment.

Indexed as

Cell MovementCell ProliferationSignal TransductionAnimalsCell LineCytoglobinFibroblastsGlobinsMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCygb protein, mouseCytoglobinGlobinsmTOR protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCell migrationCytoglobinMicroarrayTumor suppressorWound healing

Identifiers

PMID28620820
OpenAlexW2626605844

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.