Evidence map›Paper›PMID 31253779›Full record

ArticleNature communications2019

TSPAN8 promotes cancer cell stemness via activation of sonic Hedgehog signaling.

Rongxuan Zhu, Olivier Gires, Liqun Zhu, Jun Liu, Junjian Li, Hao Yang, Gaoda Ju, Jing Huang, Weiyu Ge, Yi Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
7.7field-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

110 citing papers in PubMed, 193 citations in OpenAlex.

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50 more citing papers are in PubMed but not listed here.

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

12 authors at 8 institutions in 2 countries.

Rongxuan ZhuDepartment of Oncology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Olivier GiresDepartment of Otorhinolaryngology, Head and Neck Surgery, Grosshadern Medical Center, Ludwig-Maximilians-University of Munich, Munich, Germany.
Liqun ZhuLiyang People's Hospital, Liyang, Jiangsu, 213300, China.
Jun LiuDepartment of Breast-Thyroid-Vascular Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Junjian LiDepartment of Oncology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Hao YangShanghai Key Laboratory of Molecular Imaging, Shanghai University of Medicine and Health Sciences, Shanghai, 201318, China.
Gaoda JuDepartment of Oncology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Jing HuangSchool of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, 116024, China.
Weiyu GeDepartment of Oncology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Yi ChenDivision of Anti-Tumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Zhimin LuZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, 310029, China. zhiminlu@zju.edu.cn.
Hongxia WangDepartment of Oncology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China. whx365@126.com.
Shanghai Jiao Tong University · CNShanghai First People's Hospital · CNDalian University of Technology · CNLishui City People's Hospital · CNLudwig-Maximilians-Universität München · DEShanghai Institute of Materia Medica · CNShanghai University of Medicine and Health Sciences · CNZhejiang University · CN

Funding

Shanghai Science and Technology Development Foundation (Shanghai Science and Technology Development Fund) 17JC1404400
6 · The paper itself

Abstract

Cancer stem cells (CSCs) represent a major source of treatment resistance and tumor progression. However, regulation of CSCs stemness is not entirely understood. Here, we report that TSPAN8 expression is upregulated in breast CSCs, promotes the expression of the stemness gene NANOG, OCT4, and ALDHA1, and correlates with therapeutic resistance. Mechanistically, TSPAN8 interacts with PTCH1 and inhibits the degradation of the SHH/PTCH1 complex through recruitment of deubiquitinating enzyme ATXN3. This results in the translocation of SMO to cilia, downstream gene expression, resistance of CSCs to chemotherapeutic agents, and enhances tumor formation in mice. Accordingly, expression levels of TSPAN8, PTCH1, SHH, and ATXN3 are positively correlated in human breast cancer specimens, and high TSPAN8 and ATXN3 expression levels correlate with poor prognosis. These findings reveal a molecular basis of TSPAN8-enhanced Sonic Hedgehog signaling and highlight a role for TSPAN8 in promoting cancer stemness.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHedgehog ProteinsHumansMiceMice, NudeNeoplasms, ExperimentalNeoplastic Stem CellsRNA InterferenceRNA, Small InterferingSignal TransductionTetraspaninsHedgehog ProteinsRNA, Small InterferingSHH protein, humanTetraspaninsTSPAN8 protein, human

Identifiers

PMID31253779
PMCPMC6599078
OpenAlexW2953836551

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.