Evidence map›Paper›PMID 32260399›Full record

ArticleCells2020

Sphingosine Kinase 1 Regulates the Survival of Breast Cancer Stem Cells and Non-stem Breast Cancer Cells by Suppression of STAT1.

Ling-Wei Hii, Felicia Fei-Lei Chung, Chun Wai Mai, Zong Yang Yee, Hong Hao Chan, Vijay Joseph Raja, Noah Elias Dephoure, Nigel J Pyne, Susan Pyne, Chee-Onn Leong

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

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  15. Emerging Roles of Ceramides in Breast Cancer Biology and Therapy.International journal of molecular sciences · 2022
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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

10 authors at 4 institutions in 4 countries.

Ling-Wei HiiCentre for Cancer and Stem Cell Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
Felicia Fei-Lei ChungMechanisms of Carcinogenesis Section (MCA), Epigenetics Group (EGE) International Agency for Research on Cancer, World Health Organization, 69372 Lyon, France.
Chun Wai MaiCentre for Cancer and Stem Cell Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
Zong Yang YeeCentre for Cancer and Stem Cell Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
Hong Hao ChanCentre for Cancer and Stem Cell Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
Vijay Joseph RajaDepartment of Biochemistry, Weill Cornell Medical College, New York, NY 10021, USA.
Noah Elias DephoureDepartment of Biochemistry, Weill Cornell Medical College, New York, NY 10021, USA.
Nigel J PyneStrathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow G4 0RE, Scotland, UK.
Susan PyneStrathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow G4 0RE, Scotland, UK.
Chee-Onn LeongCentre for Cancer and Stem Cell Research, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
IMU University · MYCornell University · USUniversity of Strathclyde · GBCentre international de recherche sur le cancer · FR

Funding

World Health Organization 001
6 · The paper itself

Abstract

Cancer stem cells (CSCs) represent rare tumor cell populations capable of self-renewal, differentiation, and tumor initiation and are highly resistant to chemotherapy and radiotherapy. Thus, therapeutic approaches that can effectively target CSCs and tumor cells could be the key to efficient tumor treatment. In this study, we explored the function of SPHK1 in breast CSCs and non-CSCs. We showed that RNAi-mediated knockdown of SPHK1 inhibited cell proliferation and induced apoptosis in both breast CSCs and non-CSCs, while ectopic expression of SPHK1 enhanced breast CSC survival and mammosphere forming efficiency. We identified STAT1 and IFN signaling as key regulatory targets of SPHK1 and demonstrated that an important mechanism by which SPHK1 promotes cancer cell survival is through the suppression of STAT1. We further demonstrated that SPHK1 inhibitors, FTY720 and PF543, synergized with doxorubicin in targeting both breast CSCs and non-CSCs. In conclusion, we provide important evidence that SPHK1 is a key regulator of cell survival and proliferation in breast CSCs and non-CSCs and is an attractive target for the design of future therapies.

Indexed as

ApoptosisBreast NeoplasmsCell LineageCell Line, TumorCell ProliferationCell SurvivalDoxorubicinFemaleHEK293 CellsHumansInterferonsLysophospholipidsNeoplastic Stem CellsPhosphotransferases (Alcohol Group Acceptor)Protein Kinase InhibitorsProteomicsDoxorubicinInterferonsLysophospholipidsPhosphotransferases (Alcohol Group Acceptor)Protein Kinase InhibitorsSphingosinesphingosine 1-phosphateSphingosine KinaseSTAT1 protein, humanSTAT1 Transcription Factorcancer stem cellsdrug synergismmammospheressphingolipidssphingosine kinaseSTAT1

Identifiers

PMID32260399
PMCPMC7226795
OpenAlexW3014456715

What OpenQuestion holds

Textmetadata
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.