Evidence map›Paper›PMID 35829796›Full record

ArticleAnnals of surgical oncology2022

Metabolomic Analysis Reveals that SPHK1 Promotes Oral Squamous Cell Carcinoma Progression through NF-κB Activation.

Chen-Xing Hou, Guang-Yan Mao, Qiu-Wangyue Sun, Ying Meng, Qing-Hai Zhu, Yu-Ting Tang, Wei Han, Nan-Nan Sun, Xiao-Meng Song, Chen-Xing Wang and 1 more

Abstract read
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In one paragraph

Article in Annals of surgical oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 9 citations in OpenAlex.

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  7. [Sphingosine kinase-1 regulates migration and invasion of gastric cancer cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    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

11 authors at 2 institutions in 1 country.

Chen-Xing Hou *Jiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China.
Guang-Yan Mao *Jiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China.
Qiu-Wangyue Sun *Jiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China.
Ying MengJiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China.
Qing-Hai ZhuJiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China.
Yu-Ting TangJiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China.
Wei HanJiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China.
Nan-Nan SunJiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China.
Xiao-Meng SongJiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China.
Chen-Xing WangJiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China. doctorwcx@njmu.edu.cn.
Jin-Hai YeJiangsu Key Laboratory of Oral Disease, & Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing, China. yejinhai@njmu.edu.cn.ORCID http://orcid.org/0000-0002-3789-551X
Nanjing Medical University · CNTongren Hospital · CN

Funding

Jiangsu Provincial Medical Key Talent Project ZDRCA2016087Priority Academic Program Development of Jiangsu Higher Education Institutions 2018-87Priority Academic Program Development of Jiangsu Higher Education Institutions PAPDSoutheast University-Nanjing Medical University Cooperative Research Project 2017DN03
6 · The paper itself

Abstract

backgroundMetabolic disorders are significant in the occurrence and development of malignant tumors. Changes of specific metabolites and metabolic pathways are molecular therapeutic targets. This study aims to determine the metabolic differences between oral squamous cell carcinoma (OSCC) tissues and paired adjacent noncancerous tissues (ANT) through liquid chromatography-mass spectrometry (LC-MS). SPHK1 is a key enzyme in sphingolipid metabolism. This study also investigates the potential role of SPHK1 in OSCC. MATERIALS AND

methodsThis study used LC-MS to analyze metabolic differences between OSCC tissues and paired ANT. Principal component analysis (PCA) and partial least-squares discriminant analysis (PLS-DA) were applied to explain the significance of phospholipid metabolism pathways in the occurrence and development of OSCC. Through further experiments, we confirmed the oncogenic phenotypes of SPHK1 in vitro and in vivo, including proliferation, migration, and invasion.

resultsThe sphingolipid metabolic pathway was significantly activated in OSCC, and the key enzyme SPHK1 was significantly upregulated in oral cancer tissues, predicting poor OSCC prognosis. In this study, SPHK1 overexpression was associated with high-grade malignancy and poor OSCC prognosis. SPHK1 targeted NF-κB by facilitating p65 expression to regulate OSCC tumor progression and promote metastasis.

conclusionsThis study identified metabolic differences between OSCC and paired ANT, explored the carcinogenic role of overexpressed SPHK1, and revealed the association of SPHK1 with poor OSCC prognosis. SPHK1 targets NF-κB signaling by facilitating p65 expression to regulate tumor progression and promote tumor metastasis, providing potential therapeutic targets for diagnosing and treating oral tumors.

Indexed as

Mouth NeoplasmsPhosphotransferases (Alcohol Group Acceptor)Squamous Cell Carcinoma of Head and NeckCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansNF-kappa BPhospholipidsSphingolipidsSphingosine KinaseNF-kappa BPhospholipidsPhosphotransferases (Alcohol Group Acceptor)SphingolipidsSphingosine Kinase

Identifiers

PMID35829796
OpenAlexW4285090651

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.