Evidence map›Paper›PMID 30334368›Full record

ArticleJournal of cellular and molecular medicine2018

STAT1 facilitates oestrogen receptor α transcription and stimulates breast cancer cell proliferation.

Yingxiang Hou, Xin Li, Qianhua Li, Juntao Xu, Huijie Yang, Min Xue, Gang Niu, Shu Zhuo, Kun Mu, Gaosong Wu and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

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  8. STAT1 suppresses the transcriptional activity of TRIM21 in gastric cancer.Journal of cancer research and clinical oncology · 2023
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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

14 authors at 5 institutions in 2 countries.

Yingxiang HouLaboratory of Molecular Oncology, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, Henan, China.
Xin LiLaboratory of Molecular Oncology, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, Henan, China.
Qianhua LiDepartment of Pathology, Shandong University School of Medicine, Jinan, Shandong, China.
Juntao XuRhil Rivers Technology (Beijing) Ltd, Beijing, China.
Huijie YangLaboratory of Molecular Oncology, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, Henan, China.
Min XueLaboratory of Molecular Oncology, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, Henan, China.
Gang NiuRhil Rivers Technology (Beijing) Ltd, Beijing, China.
Shu ZhuoDepartment of Molecular Biology, UT Southwestern Medical Center, Dallas, Texas.
Kun MuDepartment of Pathology, Shandong University School of Medicine, Jinan, Shandong, China.
Gaosong WuDepartment of Thyroid and Breast Surgery, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China.
Xiumin LiInstitute of Lung and Molecular Therapy (ILMT), Xinxiang Medical University, Xinxiang, Henan, China.
Hui WangLaboratory of Molecular Oncology, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, Henan, China.
Jian ZhuDepartment of Molecular Biology, UT Southwestern Medical Center, Dallas, Texas.ORCID 0000-0003-3596-4339
Ting ZhuangLaboratory of Molecular Oncology, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, Henan, China.
Xinxiang Medical University · CNBGI Group (China) · CNShandong University · CNSouthwestern Medical Center · USWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oestrogen receptor α (ERα) is overexpressed in two-thirds of all breast cancer cases and is involved in breast cancer development and progression. Although ERα -positive breast cancer can be effectively treated by endocrine therapy, endocrine resistance is an urgent clinical problem. Thus, further understanding of the underlying mechanisms involved in ERα signalling is critical in dealing with endocrine resistance in patients with breast cancer. In the present study, unbiased RNA sequence analysis was conducted between the MCF-7 and MCF-7 tamoxifen-resistant (LCC2) cell lines in order to identify differentially expressed genes. The whole transcriptomic data indicated that the JAK-STAT pathway is markedly up-regulated, particularly the ISGF3 complex. As the critical effectors, STAT1 and IRF9 were up-regulated 5- and 20-fold, respectively, in LCC2 cells. The biological experiments indicated that STAT1 is important for ERα signalling. Depletion of STAT1 or inhibition of STAT1 function significantly decreased levels of ERα protein, ERα -target gene expression and cell proliferation in both the MCF-7 and LCC2 cell lines. Chromatin immunoprecipitation revealed that ERα transcription is associated with STAT1 recruitment to the ERα promoter region, suggesting that transcriptional regulation is one mechanism by which STAT1 regulates ERα mRNA levels and ERα signalling in breast cancer cells. The present study reveals a possible endocrine-resistant mechanism by which STAT1 modulates ERα signalling and confers tamoxifen resistance. Targeting of STAT1 is a potential treatment strategy for endocrine-resistant breast cancers.

Indexed as

Transcription, GeneticBreast NeoplasmsCell ProliferationDrug Resistance, NeoplasmEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHumansInterferon-Stimulated Gene Factor 3, alpha SubunitMCF-7 CellsSignal TransductionSTAT1 Transcription FactorTamoxifenESR1 protein, humanEstrogen Receptor alphaInterferon-Stimulated Gene Factor 3, alpha SubunitSTAT1 protein, humanSTAT1 Transcription FactorTamoxifenbreast cancerERαSTAT1transcription

Identifiers

PMID30334368
PMCPMC6237559
OpenAlexW2896466576

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.