Evidence map›Paper›PMID 29605826›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

Triple Negative Breast Cancer Depends on Sphingosine Kinase 1 (SphK1)/Sphingosine-1-Phosphate (S1P)/Sphingosine 1-Phosphate Receptor 3 (S1PR3)/Notch Signaling for Metastasis.

Shushu Wang, Yueyang Liang, Wenxiao Chang, Baoquan Hu, Yi Zhang

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 57 citations in OpenAlex.

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  10. Upregulation of sphingosine kinase 1 in response to doxorubicin generates an angiogenic response via stabilization of Snail.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
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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 3 institutions in 1 country.

Shushu WangBreast Disease Center, Southwest Hospital, Third Military Medical University, Chongqing, China (mainland).
Yueyang LiangBreast Disease Center, Southwest Hospital, Third Military Medical University, Chongqing, China (mainland).
Wenxiao ChangOutpatient Department of Stomatology, Shan Xi Da Yi Hospital, Taiyuan, Shanxi, China (mainland).
Baoquan HuBreast Disease Center, Southwest Hospital, Third Military Medical University, Chongqing, China (mainland).
Yi ZhangBreast Disease Center, Southwest Hospital, Third Military Medical University, Chongqing, China (mainland).
Southwest Hospital · CNArmy Medical University · CNShanxi Dayi Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Triple negative breast cancer (TNBC) has a more aggressive recurrence. Previous reports have demonstrated that sphingosine kinase 1 (SphK1) is a crucial regulator of breast cancer progression. However, the correlation of SphK1 with clinical prognosis has been poorly investigated. Thus, we aimed to elaborate the role of SphK1 in TNBC metastasis. MATERIAL AND METHODS We first determined the level of SphK1 in breast cancer tissue samples and breast cancer cells. Furthermore, the expression of HER2 and phosphor-SphK1 (pSphK1) in human breast cancer tissue samples was determined by immunohistochemical analysis. Associations between SphK1 and clinical parameters of tumors were analyzed. The activity of SphK1 was measured by fluorescence analysis. Extracellular sphingosine-1-phosphate (S1P) was detected using an ELISA kit. Associations between SphK1 and metastasis potential were analyzed by Transwell assay. RESULTS Levels of SphK1 in TNBC patients were significantly higher than levels in other patients with other breast tumors. The expression of SphK1 was positively correlated with poor overall survival (OS) and progression-free survival (PFS), as well as poor response to 5-FU and doxorubicin. The depression of SphK1 thus could repress the Notch signaling pathway, reduce migration, and invasion of TNBC cells in vivo and in vitro. Furthermore, silencing of SphK1 by Ad-SPHK1-siRNA or SphK1 inhibitor PF543 sensitized TNBCs to 5-FU and doxorubicin. Our results also indicated that SphK1 inhibition could effectively counteracts tumors metastasis via Notch signaling pathways, indicating a potentially anti-tumor strategy in TNBC. CONCLUSIONS We found that elevated levels of pSphK1 were positive correlation with high expression of S1P, which in turn promoted metastasis of TNBC through S1P/S1PR3/Notch signaling pathway.

Indexed as

AnimalsCell Line, TumorDoxorubicinDrug SynergismErb-b2 Receptor Tyrosine KinasesFemaleFluorouracilHeterograftsHumansLysophospholipidsMCF-7 CellsMethanolMiceMice, Inbred NODMice, SCIDMiddle AgedDoxorubicinERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesFluorouracilLysophospholipidsMethanolPF-543Phosphotransferases (Alcohol Group Acceptor)PyrrolidinesReceptors, LysosphingolipidReceptors, NotchSphingosinesphingosine 1-phosphatesphingosine-1-phosphate receptor-3, humanSphingosine-1-Phosphate ReceptorsSphingosine KinaseSulfones

Identifiers

PMID29605826
PMCPMC5894569
OpenAlexW2795157171

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.