Evidence map›Paper›PMID 31115571›Full record

ArticleMolecular medicine reports2019

Formaldehyde induces the apoptosis of BMCs of BALB/c mice via the PTEN/PI3K/Akt signal transduction pathway.

Guangyan Yu, Chunhua Wang, Xiangfu Song, Shimeng Liu, Yixin Zhang, Lida Fan, Yixue Yang, Yulu Huang, Jiayi Song

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 10 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

9 authors at 1 institution in 1 country.

Guangyan YuDepartment of Preventive Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
Chunhua WangDepartment of Preventive Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
Xiangfu SongDepartment of Preventive Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
Shimeng LiuDepartment of Preventive Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
Yixin ZhangDepartment of Preventive Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
Lida FanDepartment of Preventive Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
Yixue YangDepartment of Preventive Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
Yulu HuangDepartment of Preventive Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
Jiayi SongDepartment of Preventive Medicine, School of Public Health, Jilin University, Changchun, Jilin 130021, P.R. China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The International Agency for Research on Cancer has classified formaldehyde (FA) as a leukemogen to humans in 2012; however, the underlying mechanism remains unclear. Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor‑suppressor gene and can negatively regulate the phosphoinositide 3‑kinase (PI3K)/protein kinase B (Akt) signal transduction pathway, which is associated with cell proliferation, apoptosis and carcinogenesis. To determine the association between FA and the PTEN/PI3K/Akt signal transduction pathway, flow cytometry, reverse transcription‑quantitative polymerase chain reaction, western blotting and immunohistochemical analysis were conducted. Bone marrow cells were obtained from BALB/c mice, divided into the control (untreated cells) and FA groups, which were treated with various doses of FA (50, 100 and 200 µmol/l). Following treatment with FA for 24 h, cell viability, the cell cycle, apoptosis, and the expression of PTEN, PI3K and Akt, as well as the protein expression of B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X (Bax), and Caspases‑3 and ‑9 were examined. Furthermore, 10 µmol/PI3K inhibitor (LY294002) was applied to inhibit the PTEN/PI3K/Akt signal transduction pathway and 100 µmol/l FA was selected for treatment; alteration in the cell cycle were analyzed. The results demonstrated that FA could suppress cell viability, and downregulate PTEN and Bcl‑2; the expression of PI3K, Akt, Bax, and Caspases‑3 and ‑9 were upregulated. Additionally, FA was reported to induce cell cycle arrest at the G0/G1 phase and apoptosis. Following the application of LY294002 to inhibit the PTEN/PI3K/Akt signal transduction pathway, the numbers of cells arrested in the G0/G1 phase were significantly increased in the PI3K inhibitor group compared with the control (P<0.01); however, no significant change in the number of G0/G1 cells compared with FA group was observed (P>0.05). The results of the present study suggested that the PTEN/PI3K/Akt signal transduction pathway served an important role in the process of FA‑induced apoptosis, which may be associated with regulating the cell cycle; thus, cell proliferation may be affected.

Indexed as

AnimalsApoptosisBone Marrow CellsCell Cycle CheckpointsCell ProliferationCell SurvivalChromonesFormaldehydeGene Expression Regulation, NeoplasticHumansMiceMorpholinesNeoplasm ProteinsNeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesFormaldehydeMorpholinesNeoplasm ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID31115571
PMCPMC6580029
OpenAlexW2944000672

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Registered trials

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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.