Evidence map›Paper›PMID 38031089›Full record

ArticleJournal of translational medicine2023

SIX1 amplification modulates stemness and tumorigenesis in breast cancer.

Liantao Guo, Faminzi Li, Hanqing Liu, Deguang Kong, Chuang Chen, Shengrong Sun

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 21 citations in OpenAlex.

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  12. Mechanistic study ofTranslational andrology and urology · 2025
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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

6 authors at 1 institution in 1 country.

Liantao Guo *Department of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan, 430060, Hubei, China.ORCID 0000-0003-2617-8651
Faminzi Li *Reproductive Medical Center, Renmin Hospital of Wuhan University and Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, No. 238 Jiefang Road, Wuchang District, Wuhan, 430060, Hubei, China.
Hanqing LiuDepartment of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan, 430060, Hubei, China.
Deguang KongDepartment of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan, 430060, Hubei, China. 2016103030008@whu.edu.cn.
Chuang ChenDepartment of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan, 430060, Hubei, China. chen0678@126.com.
Shengrong SunDepartment of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan, 430060, Hubei, China. sun137@sina.com.
Wuhan University · CN

Funding

National Natural Science Foundation of China No.8210114078
6 · The paper itself

Abstract

backgroundSine oculis homeobox homolog 1 (SIX1) is a transcription factor that has recently been identified as a crucial regulator of embryonic development and tumorigenesis. SIX1 is upregulated in different types of tumors, including breast cancer. However, the role and mechanism of SIX1 upregulation in breast cancer carcinogenesis remains uncertain.

methodsIn this study, we utilized various databases such as UALCAN, TCGA, STRING, and Kaplan-Meier Plotter to investigate the mRNA expression, prognosis, transcriptional profile changes, signal pathway rewiring, and interaction with cancer stem cells of SIX1 in breast cancer. We also conducted both in vitro and in vivo experiments to validate its positive regulation effect on breast cancer stem cells.

resultsOur findings demonstrated that the expression of SIX1 varies among different subtypes of breast cancer and that it upregulates breast cancer grading and lymph node metastasis. Besides, SIX1 participates in the rewiring of several cancer signaling pathways, including estrogen, WNT, MAPK, and other pathways, and interacts with cancer stem cells. SIX1 showed a significant positive correlation with breast cancer stem cell markers such as ALDH1A1, EPCAM, ITGB1, and SOX2. Moreover, our in vitro and in vivo experiments confirmed that SIX1 can promote the increase in the proportion of stem cells and tumor progression.

conclusionsAltogether, our results suggest that SIX1 plays an essential regulatory role in breast cancer's occurrence, and its amplification can be utilized as a diagnostic and prognostic predictor. The interaction between SIX1 and cancer stem cells may play a critical role in regulating breast cancer's initiation and metastasis.

Indexed as

Breast NeoplasmsHomeodomain ProteinsCarcinogenesisCell Line, TumorCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHumansTranscription FactorsHomeodomain ProteinsSIX1 protein, humanTranscription FactorsBreast cancerCancer stem cellsMetastasisSIX1Tumorigenesis

Identifiers

PMID38031089
PMCPMC10685563
OpenAlexW4389149301

What Socratic holds

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LicenceCC BY
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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 Socratic graph.