Evidence map›Paper›PMID 23291272›Full record

ArticleCarcinogenesis2013

The oncoprotein HBXIP activates transcriptional coregulatory protein LMO4 via Sp1 to promote proliferation of breast cancer cells.

Lin Yue, Leilei Li, Fangfang Liu, Nan Hu, Weiying Zhang, Xiao Bai, Yinghui Li, Yingyi Zhang, Li Fu, Xiaodong Zhang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.0field-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

34 citing papers in PubMed, 64 citations in OpenAlex.

  1. HBXIP expression predicts patient prognosis in breast cancer.Medical oncology (Northwood, London, England) · 2014
    Trial
  2. Article
  3. Prevalence of Hepatitis B Virus Markers among the Women with Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. RNA NCancer gene therapy · 2020
    Review
  8. Article
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  11. The Complex Roles and Therapeutic Implications of mFrontiers in cell and developmental biology · 2020
    Review
  12. Article
  13. Article
  14. Acta pharmaceutica Sinica. B · 2018
    Review
  15. Article
  16. Article
  17. Article
  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

11 authors at 3 institutions in 1 country.

Lin YueDepartment of Biochemistry, College of Life Sciences, Nankai University, Tianjin, China.
Leilei Li
Fangfang Liu
Nan Hu
Weiying Zhang
Xiao Bai
Yinghui Li
Yingyi Zhang
Li Fu
Xiaodong Zhang
Lihong Ye
Nankai University · CNTianjin Medical University · CNTianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B X-interacting protein (HBXIP) is an important oncoprotein that plays critical role in the development of cancer. In this study, we report that HBXIP activates LIM-only protein 4 (LMO4), a transcriptional coregulatory protein, in promotion of cell proliferation. We observed that the messenger RNA (mRNA) expression levels of HBXIP were positively associated with those of LMO4 in clinical breast cancer tissues. We further identified that HBXIP upregulated LMO4 at the levels of promoter, mRNA and protein in MCF-7 and LM-MCF-7 breast cancer cell lines. The expression of cyclin D1 and cyclin E, downstream effectors of LMO4, could be upregulated by HBXIP through LMO4. Then, chromatin immunoprecipitation (ChIP) assay revealed that HBXIP was able to interact with the promoter region of LMO4. Electrophoretic mobility shift assay showed that HBXIP occupied the -237/-206 region of LMO4 promoter containing Sp1 binding element. The mutant of Sp1 binding site in the LMO4 promoter impeded the interaction of HBXIP with the promoter. Co-immunoprecipitation, ChIP and luciferase reporter gene assays showed that HBXIP activated LMO4 promoter through binding to Sp1. In function, flow cytometry, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, 5-ethynyl-2'-deoxyuridine (EdU) incorporation assays and animal transplantation assays demonstrated that HBXIP-enhanced cell proliferation of breast cancer through upregulating LMO4 in vitro and in vivo. Thus, we concluded that oncoprotein HBXIP is able to activate the transcriptional coregulatory protein LMO4 through transcription factor Sp1 in promotion of proliferation of breast cancer cells. HBXIP may serve as a driver gene to activate transcription in the development of cancer.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationChromatin ImmunoprecipitationCyclin D1Cyclin EDisease ProgressionElectrophoretic Mobility Shift AssayFemaleGene Expression Regulation, NeoplasticHumansLIM Domain ProteinsMCF-7 CellsMiceAdaptor Proteins, Signal TransducingCyclin D1Cyclin ELAMTOR5 protein, humanLIM Domain ProteinsLMO4 protein, humanRNA, MessengerRNA, Small InterferingSp1 Transcription Factor

Identifiers

PMID23291272
PMCPMC3616668
OpenAlexW2146238264

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.