Evidence map›Paper›PMID 28468627›Full record

ArticleLipids in health and disease2017

The omega-3 polyunsaturated fatty acid docosahexaenoic acid inhibits proliferation and progression of non-small cell lung cancer cells through the reactive oxygen species-mediated inactivation of the PI3K /Akt pathway.

Yuanqin Yin, Chengguang Sui, Fandong Meng, Ping Ma, Youhong Jiang

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 90 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 1 institution in 1 country.

Yuanqin YinCancer Institute, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, 110001, China. doustar88@126.com.
Chengguang SuiCancer Institute, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, 110001, China.
Fandong MengCancer Institute, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, 110001, China.
Ping MaCancer Institute, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, 110001, China.
Youhong JiangCancer Institute, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, 110001, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDocosahexaenoic acid(DHA) inhibits tumor growth and progression in various cancers, including lung cancer. However, the mechanisms involved remain unclear. The aim of this study was to identify the mechanism of DHA in inhibiting progression of non-small cell lung cancer (NSCLC) in vitro.

methodsThe proliferation of A549 was tested by MTT, and cell apoptosis was analysed using flow cytometer. The migration and invasion were examined respectively by wound healing assay and Transwell invasion assay. The level of ROS (reactive oxygen species, ROS) was checked by DCF (dichlorodihydrofluorescein, DCF) production in cells. The apoptosis associated protein (caspase-3, PARP,Bax,Bcl-2 and survivin) and metastases associated proteins including HEF1, MMP9 and VEGF were detected by Western blot, and the same method was used in the expression of PI3K and Akt.

resultsDHA inhibited proliferation and induced apoptosis of A549 cells. Moreover, it suppressed the invasion and metastasis of A549 cells, while downregulating the levels of metastasis-associated proteins, including HEF1, matrix metallopeptidase (MMP9), and vascular endothelial growth factor (VEGF), in a dose -dependent manner. In addition, DHA inactivated Akt phosphorylation. All of these responses were associated with the accumulation of intracellular ROS. DHA downregulated the level of antioxidant enzymes such as catalase, while the antioxidant N-acetyl-cysteine (NAC) reversed the effect of DHA, which further validated our findings.

conclusionsThe present study demonstrates that DHA inhibits the development of non-small lung tumors through an ROS-mediated inactivation of the PI3K/Akt signaling pathway.

Indexed as

Gene Expression Regulation, NeoplasticA549 CellsAdaptor Proteins, Signal TransducingAntineoplastic AgentsApoptosisCaspase 3CatalaseCell MovementCell ProliferationCell SurvivalDocosahexaenoic AcidsHumansInhibitor of Apoptosis ProteinsMatrix Metalloproteinase 9Phosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsAdaptor Proteins, Signal TransducingAntineoplastic AgentsBCL2 protein, humanBIRC5 protein, humanCASP3 protein, humanCaspase 3CatalaseDocosahexaenoic AcidsInhibitor of Apoptosis ProteinsMatrix Metalloproteinase 9MMP9 protein, humanNEDD9 protein, humanPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphoproteinsPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesSurvivinVascular Endothelial Growth Factor AVEGFA protein, humanInvasionLung cancerMigrationProliferationReactive oxygen species

Identifiers

PMID28468627
PMCPMC5415787
OpenAlexW2610366558

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.