Evidence map›Paper›PMID 28206952›Full record

ArticleOncotarget2017

Identification of sphingosine kinase 1 (SphK1) as a primary target of icaritin in hepatocellular carcinoma cells.

Pei-Hua Lu, Min-Bin Chen, Yuan-Yuan Liu, Mian-Hua Wu, Wen-Ting Li, Mu-Xin Wei, Chao-Ying Liu, Shu-Kui Qin

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  14. A comparative study on theDrug delivery · 2020
    Article
  15. Article
  16. Article
  17. Article
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  20. Review
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

8 authors at 4 institutions in 1 country.

Pei-Hua LuDepartment of Medical Oncology, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China.
Min-Bin ChenDepartment of Oncology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, China.
Yuan-Yuan LiuDepartment of Oncology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, China.
Mian-Hua WuJiangsu Collaborative Innovation Center of Traditional Chinese Medicine (TCM) Prevention and Treatment of Tumor of Nanjing University of Chinese Medicine, Nanjing, China.
Wen-Ting LiJiangsu Collaborative Innovation Center of Traditional Chinese Medicine (TCM) Prevention and Treatment of Tumor of Nanjing University of Chinese Medicine, Nanjing, China.
Mu-Xin WeiDepartment of Traditional Chinese Medicine, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Chao-Ying LiuDepartment of Medical Oncology, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China.
Shu-Kui QinPeople's Liberation Army Cancer Center, 81st Hospital of People's Liberation Army, Nanjing, China.
Jiangsu University · CNNanjing Medical University · CNNanjing University of Chinese Medicine · CNNanjing Traditional Chinese Medicine Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a highly aggressive neoplasm. We aim to explore the anti-HCC activity by a natural prenylflavonoid icaritin. Icaritin was cytotoxic and pro-apoptotic when added to established (HepG2, KYN-2 and Huh-7 lines) and primary human HCC cells. At the signaling level, icaritin inhibited sphingosine kinase 1 (SphK1) activity in HCC cells, which led to pro-apoptotic ceramide production and JNK1 activation. SphK1 inhibition or silence (by shRNA/microRNA) mimicked icaritin-mediated cytotoxicity, and almost nullified icaritin's activity in HepG2 cells. Reversely, exogenous over-expression of SphK1 sensitized icaritin-induced HepG2 cell apoptosis. In vivo, oral administration of icaritin dramatically inhibited HepG2 xenograft growth in SCID mice. Further, SphK1 activity in icaritin-treated tumors was largely inhibited. In summary, icaritin exerts potent anti-HCC activity in vitro and in vivo. SphK1 inhibition could be the primary mechanism of its actions in HCC cells.

Indexed as

AnimalsApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell ProliferationCeramidesFlavonoidsGene Expression Regulation, EnzymologicHumansLiver NeoplasmsMaleMiceMice, SCIDMiddle AgedPhosphotransferases (Alcohol Group Acceptor)Signal TransductionBiomarkers, TumorCeramidesFlavonoidsicaritinPhosphotransferases (Alcohol Group Acceptor)Sphingosine Kinasehepatocellular carcinoma (HCC)icaritinsphingosine kinase 1 (SphK1) and ceramide

Identifiers

PMID28206952
PMCPMC5410263
OpenAlexW2589036102

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.