Evidence map›Paper›PMID 30204129›Full record

ArticleThe Journal of clinical investigation2018

HIC1 deletion promotes breast cancer progression by activating tumor cell/fibroblast crosstalk.

Yingying Wang, Xiaoling Weng, Luoyang Wang, Mingang Hao, Yue Li, Lidan Hou, Yu Liang, Tianqi Wu, Mengfei Yao, Guowen Lin and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
2.7field-weighted citation impact, top 7% 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

59 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. [Temporal changes of chronic postsurgical pain in mice: the regulatory role of CX3CL1 in the dorsal root ganglion].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
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  12. Review
  13. Exploring G Protein-Coupled Receptors in Hematological Cancers.ACS pharmacology & translational science · 2024
    Article
  14. Neddylation steers the fate of cellular receptors.Experimental & molecular medicine · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. International journal of molecular sciences · 2024
    Article
  19. Integration Analysis of Single-Cell Multi-Omics Reveals Prostate Cancer Heterogeneity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    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

16 authors at 6 institutions in 2 countries.

Yingying WangDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaoling WengCancer Institute, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Luoyang WangDepartment of Chemical Engineering, Tsinghua University, Beijing, China.
Mingang HaoDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Yue LiPathology Center, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lidan HouDepartment of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yu LiangDepartment of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Tianqi WuCancer Institute, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Mengfei YaoCancer Institute, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Guowen LinDepartment of Urology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Yiwei JiangDepartment of Breast Surgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Guohui FuPathology Center, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhaoyuan HouDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiangjun MengDepartment of Gastroenterology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jinsong LuDepartment of Breast Surgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jianhua WangCancer Institute, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Shanghai Jiao Tong University · CNFudan University Shanghai Cancer Center · CNRenji Hospital · CNAnhui University of Science and Technology · CNTsinghua University · CNUniversity of Cincinnati Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BrCa) is the malignant tumor that most seriously threatens female health; however, the molecular mechanism underlying its progression remains unclear. Here, we found that conditional deletion of hypermethylated in cancer 1 (HIC1) in the mouse mammary gland might contribute to premalignant transformation in the early stage of tumor formation. Moreover, the chemokine (C-X-C motif) ligand 14 (CXCL14) secreted by HIC1-deleted BrCa cells bound to its cognate receptor GPR85 on mammary fibroblasts in the microenvironment and was responsible for activating these fibroblasts via the ERK1/2, Akt, and neddylation pathways, whereas the activated fibroblasts promoted BrCa progression via the induction of epithelial-mesenchymal transition (EMT) by the C-C chemokine ligand 17 (CCL17)/CC chemokine receptor 4 (CCR4) axis. Finally, we confirmed that the HIC1-CXCL14-CCL17 loop was associated with the malignant progression of BrCa. Therefore, the crosstalk between HIC1-deleted BrCa cells and mammary fibroblasts might play a critical role in BrCa development. Exploring the progression of BrCa from the perspective of microenvironment will be beneficial for identifying the potential prognostic markers of breast tumor and providing more effective treatment strategies.

Indexed as

Breast NeoplasmsFibroblastsNeoplasm ProteinsAnimalsCell CommunicationEpithelial-Mesenchymal TransitionFemaleGene DeletionHumansKruppel-Like Transcription FactorsMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, KnockoutSignal TransductionTumor MicroenvironmentHIC1 protein, humanHic1 protein, mouseKruppel-Like Transcription FactorsNeoplasm ProteinsBreast cancerCell BiologyChemokinesOncology

Identifiers

PMID30204129
PMCPMC6264654
OpenAlexW2891254176

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.