Evidence map›Paper›PMID 32724162›Full record

ArticleOncogene2020

Extracellular ATP promotes breast cancer invasion and chemoresistance via SOX9 signaling.

Hui Yang, Yue-Hang Geng, Peng Wang, Han Yang, Yan-Ting Zhou, Hong-Quan Zhang, Hui-Ying He, Wei-Gang Fang, Xin-Xia Tian

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  3. Direct targeting of GLUT1 in cancer: A decade of inhibitor discovery and medicinal chemistry insights.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
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  12. Regulatory role of CD39 and CD73 in tumor immunity.Future oncology (London, England) · 2024
    Review
  13. Review
  14. Review
  15. The ATP-dependent Pathways and Human Diseases.Current medicinal chemistry · 2023
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

9 authors at 1 institution in 2 countries.

Hui YangDepartment of Pathology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), School of Basic Medical Sciences, Third Hospital, Peking University Health Science Center, Beijing 100191, China.ORCID http://orcid.org/0000-0002-9138-1325
Yue-Hang GengDepartment of Pathology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), School of Basic Medical Sciences, Third Hospital, Peking University Health Science Center, Beijing 100191, China.
Peng WangDepartment of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing 100191, China.ORCID http://orcid.org/0000-0002-2558-292X
Han YangDepartment of Pathology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), School of Basic Medical Sciences, Third Hospital, Peking University Health Science Center, Beijing 100191, China.
Yan-Ting ZhouDepartment of Pathology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), School of Basic Medical Sciences, Third Hospital, Peking University Health Science Center, Beijing 100191, China.
Hong-Quan ZhangDepartment of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing 100191, China.
Hui-Ying HeDepartment of Pathology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), School of Basic Medical Sciences, Third Hospital, Peking University Health Science Center, Beijing 100191, China.
Wei-Gang FangDepartment of Pathology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), School of Basic Medical Sciences, Third Hospital, Peking University Health Science Center, Beijing 100191, China. wgfang@bjmu.edu.cn.
Xin-Xia TianDepartment of Pathology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), School of Basic Medical Sciences, Third Hospital, Peking University Health Science Center, Beijing 100191, China. tianxinxia@bjmu.edu.cn.ORCID http://orcid.org/0000-0002-1593-4987
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous research demonstrated that extracellular adenosine 5'-triphosphate (ATP) could promote breast cancer cell invasion. However, the impact of extracellular ATP on chemoresistance and the mechanisms behind ATP pro-invasion and pro-chemoresistance remain unclear. Here we aimed to determine the molecules or signaling pathways involved. cDNA microarray was performed to identify the differentially expressed genes before and after ATP treatment. As a result, Sex-determining region Y-box 9 (SOX9) was up-regulated after ATP treatment in breast cancer cells. In vitro invasion and migration assays demonstrated that knocking down SOX9 attenuated ATP-driven invasive capability. Mass spectrometry and co-IP revealed that SOX9 interacted with Janus kinase 1 (JAK1). Afterward, IL-6-JAK1-STAT3 signaling was demonstrated to promote SOX9 expression and invasion following ATP treatment. Notably, ATP-IL-6-SOX9 signaling was shown to stimulate chemoresistance in breast cancer cells. ChIP assays identified some potential SOX9 target genes, among which carcinoembryonic antigen-related cell adhesion molecule 5/6 (CEACAM5/6) was demonstrated to mediate ATP pro-invasive function, while ATP-binding cassette subfamily B member 1 (ABCB1) and ATP-binding cassette subfamily G member 2 (ABCG2) mediated ATP-driven chemoresistance. In addition, SOX9-knockdown and apyrase (an ATP hydrolase)-treated MDA-MB-231 cells illustrated decreased tumor growth and enhanced drug sensitivity in nude mice. In vitro spheroid formation assays also proved the significance of ATP-SOX9 in mediating chemoresistance. Moreover, molecules involved in ATP-SOX9 signaling were up-regulated in human breast carcinoma specimens and were associated with poor prognosis. Altogether, SOX9 signaling is vital in ATP-driven invasion and chemoresistance, which may serve as a potential target for breast cancer therapies.

Indexed as

Adenosine TriphosphateBreast NeoplasmsCell Line, TumorDrug Resistance, NeoplasmFemaleHumansSignal TransductionSOX9 Transcription FactorTransfectionAdenosine TriphosphateSOX9 protein, humanSOX9 Transcription Factor

Identifiers

PMID32724162
OpenAlexW3045843296

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.