Evidence map›Paper›PMID 34121352›Full record

ArticleCancer medicine2021

ALOX5-5-HETE promotes gastric cancer growth and alleviates chemotherapy toxicity via MEK/ERK activation.

Jianjun Tang, Chuang Zhang, Jingjing Lin, Peng Duan, Jian Long, Hongyan Zhu

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

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  13. Lipoxygenases at the Intersection of Infection and Carcinogenesis.International journal of molecular sciences · 2024
    Review
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  15. Role of ALOX5 in non-small cell lung cancer: A potential therapeutic target associated with immune cell infiltration.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
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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

6 authors at 3 institutions in 1 country.

Jianjun TangDepartment of General Surgery, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Chuang ZhangDepartment of Pediatrics, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Jingjing LinDepartment of Blood Transfusion, Xiangyang Traditional Chinese Medicine Hospital, Xiangyang, China.
Peng DuanDepartment of Obstetrics and Gynaecology, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Jian LongDepartment of Oncology, Jingzhou Central Hospital, The Second Clinical Medical College, Yangtze University, Jingzhou, China.ORCID 0000-0002-0332-6431
Hongyan ZhuDepartment of Oncology, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, China.
Hubei University of Medicine · CNXiangyang Hospital of Traditional Chinese Medicine · CNYangtze University · CN

Funding

Hubei Nature Science Foundation 81602306National Natural Science Foundation of China 81901567Natural Science Foundation of Hubei Province 2018CFB112Nature Science Foundation of Hubei Provincial Department of Education Q20202105
6 · The paper itself

Abstract

backgroundRecent studies highlight the regulatory role of arachidonate lipoxygenase5 (Alox5) and its metabolite 5-hydroxyeicosatetraenoic acid (5-HETE) in cancer tumorigenesis and progression. In this study, we analyzed the expression, biological function and the downstream signaling of Alox5 in gastric cancer.

methodsAlox5 protein levels were measured using IHC and ELISA. Growth, migration and survival assays were performed. Phosphorylation of molecules involved in growth and survival signaling were analyzed by WB. Analysis of variance and t-test were used for statistic analysis.

resultsAlox5 and 5-HETE levels were upregulated in gastric cancer patients. ALOX5 overexpression or 5-HETE addition activates gastric cancer cells and reduces chemotherapy's efficacy. In contrast, ALOX5 inhibition via genetic and pharmacological approaches suppresses gastric cancer cells and enhances chemotherapy's efficacy. In addition, Alox5 inhibition led to suppression of ERK-mediated signaling pathways whereas ALOX5-5-HETE activates ERK-mediated signaling in gastric cancer cells.

conclusionsOur work demonstrates the critical role of ALOX5-5-HETE in gastric cancer and provides pre-clinical evidence to initialize clinical trial using zileuton in combination with chemotherapy for treating gastric cancer.

Indexed as

Cell ProliferationAnalysis of VarianceAntineoplastic AgentsArachidonate 5-LipoxygenaseCell SurvivalDisease ProgressionHumansHydroxyeicosatetraenoic AcidsHydroxyureaLipoxygenase InhibitorsMAP Kinase Signaling SystemPhosphorylationStomach NeoplasmsUp-Regulation5-hydroxy-6,8,11,14-eicosatetraenoic acidALOX5 protein, humanAntineoplastic AgentsArachidonate 5-LipoxygenaseHydroxyeicosatetraenoic AcidsHydroxyureaLipoxygenase Inhibitorszileuton5-HETEAlox5chemotherapygastric cancerMEK/ERKzileuton

Identifiers

PMID34121352
PMCPMC8335819
OpenAlexW3169925532

What OpenQuestion holds

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LicenceCC BY
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.