Evidence map›Paper›PMID 20504375›Full record

ArticleMolecular cancer2010

HOXB13 promotes androgen independent growth of LNCaP prostate cancer cells by the activation of E2F signaling.

Young-Rang Kim, Kyung-Jin Oh, Ra-Young Park, Nguyen Thi Xuan, Taek-Won Kang, Dong-Deuk Kwon, Chan Choi, Min Soo Kim, Kwang Il Nam, Kyu Youn Ahn and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  6. Distinct transcription factor interactions drive HOXB13 activity in different stages of prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  15. TRAF4-mediated nonproteolytic ubiquitination of androgen receptor promotes castration-resistant prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Article
  17. Review
  18. SWI/SNF chromatin remodelers in prostate cancer progression.Frontiers in epigenetics and epigenomics · 2023
    Review
  19. Article
  20. Review
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 2 institutions in 1 country.

Young-Rang KimDepartment of Anatomy, Chonnam National University Medical School, Gwangju, Korea.
Kyung-Jin Oh
Ra-Young Park
Nguyen Thi Xuan
Taek-Won Kang
Dong-Deuk Kwon
Chan Choi
Min Soo Kim
Kwang Il Nam
Kyu Youn Ahn
Chaeyong Jung
Chonnam National University · KRChonnam National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAndrogen signaling plays a critical role in the development of prostate cancer and its progression. However, androgen-independent prostate cancer cells emerge after hormone ablation therapy, resulting in significant clinical problems. We have previously demonstrated that the HOXB13 homeodomain protein functions as a prostate cancer cell growth suppressor by inhibiting androgen-mediated signals. However, the role of the HOXB13 in androgen-independent growth of prostate cancer cells remains unexplained.

resultsIn this report, we first demonstrated that HOXB13 was highly overexpressed in hormone-refractory tumors compared to tumors without prostate-specific antigen after initial treatment. Functionally, in an androgen-free environment minimal induction of HOXB13 in LNCaP prostate cancer cells, to the level of the normal prostate, markedly promoted cell proliferation while suppression inhibited cell proliferation. The HOXB13-mediated cell growth promotion in the absence of androgen, appears to be mainly accomplished through the activation of RB-E2F signaling by inhibiting the expression of the p21waf tumor suppressor. Indeed, forced expression of HOXB13 dramatically decreased expression of p21waf; this inhibition largely affected HOXB13-mediated promotion of E2F signaling.

conclusionsTaken together, the results of this study demonstrated the presence of a novel pathway that helps understand androgen-independent survival of prostate cancer cells. These findings suggest that upregulation of HOXB13 is associated with an additive growth advantage of prostate cancer cells in the absence of or low androgen concentrations, by the regulation of p21-mediated E2F signaling.

Indexed as

AgedAged, 80 and overAntibody SpecificityBlotting, WesternCell Line, TumorCyclin-Dependent Kinase Inhibitor p21E2F Transcription FactorsHomeodomain ProteinsHumansImmunohistochemistryMaleMiddle AgedProstatic NeoplasmsReceptors, AndrogenReverse Transcriptase Polymerase Chain ReactionSignal TransductionCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21E2F Transcription FactorsHomeodomain ProteinsHOXB13 protein, humanReceptors, Androgen

Identifiers

PMID20504375
PMCPMC2890607
OpenAlexW2172102403

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.