Evidence map›Paper›PMID 17533366›Full record

ArticleOncogene2007

Deletion of Tip30 leads to rapid immortalization of murine mammary epithelial cells and ductal hyperplasia in the mammary gland.

J Pecha, D Ankrapp, C Jiang, W Tang, I Hoshino, K Bruck, K-U Wagner, H Xiao

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. SRSF3 plays a key role in liver cancer sex disparity by facilitating hepatocyte expression of ERα and FOXA.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. TIP30: A Novel Tumor-Suppressor Gene.Oncology research · 2014
    Review
  9. Article
  10. Article
  11. Article
  12. CCN5: biology and pathophysiology.Journal of cell communication and signaling · 2010
    Article
  13. CC3/TIP30 affects DNA damage repair.BMC cell biology · 2010
    Article
  14. Article
  15. Review
  16. 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

8 authors at 2 institutions in 1 country.

J PechaEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA.
D Ankrapp
C Jiang
W Tang
I Hoshino
K Bruck
K-U Wagner
H Xiao
University of Nebraska Medical Center · USMichigan State University · US

Funding

The Role of A Transcription Cofactor in TumorigenesisR01DK066110 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI XIAO, HUA · 2004 to 2008
$1.3M
NIDDK NIH HHS DK066110-01
6 · The paper itself

Abstract

Transformation of mammary epithelial cells (MECs) from the normal to the neoplastic stage requires the dysregulation of tumor suppressor genes and proto-oncogenes. Tip30 is a tumor suppressor that can inhibit estrogen receptor-mediated transcription in MECs, but its role in MEC proliferation remains unknown. Here, we show that deleting the Tip30 gene leads to ductal hyperplasia in mouse mammary glands early in life and extensive mammary hyperplasia with age. Tip30(-/-) mammary glands transplanted into wild-type mammary fat pads also display mammary trees with extensive ductal hyperplasia. Strikingly, Tip30 deletion promotes proliferation of primary MECs and results in rapid immortalization of MECs in vitro relative to wild-type cells. Gene array analysis identified significant increases in the expression of mammary epithelial growth factors Wisp2 and Igf-1 in Tip30(-/-) cells. Knockdown of either Wisp2 or Igf-1 using short interfering RNA dramatically inhibited proliferation of Tip30(-/-) cells. Together, these results suggest that Tip30 is an intrinsic and negative regulator of MEC proliferation partly through the inhibition of Wisp2 and Igf-1 expression, and its absence in the mammary gland may predispose MECs to neoplastic transformation.

Indexed as

Genes, Tumor SuppressorAcetyltransferasesAnimalsCell Growth ProcessesCell Transformation, NeoplasticEpithelial CellsFemaleGene DeletionHyperplasiaInsulin-Like Growth Factor IMammary Glands, AnimalMammary Neoplasms, ExperimentalMiceMice, Inbred C57BLMice, KnockoutRepressor ProteinsAcetyltransferasesInsulin-Like Growth Factor IRepressor ProteinsRNA, MessengerRNA, Small InterferingTip30 protein, mouseTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID17533366
OpenAlexW2106991852

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.