Evidence map›Paper›PMID 23222713›Full record

ArticleOncogene2014

Transformation of human ovarian surface epithelial cells by Krüppel-like factor 8.

H Lu, X Wang, A M Urvalek, T Li, H Xie, L Yu, J Zhao

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. The roles of FHL2 in cancer.Clinical and experimental medicine · 2023
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. KLF7: a new candidate biomarker and therapeutic target for high-grade serous ovarian cancer.Journal of experimental & clinical cancer research : CR · 2020
    Article
  10. Review
  11. Article
  12. Regulation of Krüppel-like factor 8 by the NEDD4 E3 ubiquitin ligase.American journal of translational research · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

7 authors at 3 institutions in 1 country.

H LuBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
X WangBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
A M UrvalekBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
T LiBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
H XieTranslational Research Institute for Metabolism and Diabetes, Florida Hospital, Orlando, FL, USA.
L YuBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
J ZhaoBurnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA.
University of Central Florida · USFlorida College · USTranslational Research Institute for Metabolism and Diabetes · US

Funding

KLF8 Regulation of EMT Tumor MetastasisR01CA132977 · NCI · UNIVERSITY OF CENTRAL FLORIDA · PI ZHAO, JIHE · 2009 to 2014
$1.3M
NCI NIH HHS CA132977NCI NIH HHS R01 CA132977
6 · The paper itself

Abstract

We have previously demonstrated that Krüppel-like factor 8 (KLF8) participates in oncogenic transformation of mouse fibroblasts and is highly overexpressed in human ovarian cancer. In this work, we first correlated KLF8 overexpression with the aggressiveness of ovarian patient tumors and then tested if KLF8 could transform human ovarian epithelial cells. Using the immortalized non-tumorigenic human ovarian surface epithelial cell line T80 and retroviral infection, we generated cell lines that constitutively overexpress KLF8 alone or its combination with the known ovarian oncogenes c-Myc, Stat3c and/or Akt and examined the cell lines for anchorage-independent growth and tumorigenesis. The soft agar clonogenic assay showed that T80/KLF8 cells formed significantly more colonies than the mock cells. Interestingly, the cells expressing both KLF8 and c-Myc formed the largest amounts of colonies, greater than the sum of colonies formed by the cells expressing KLF8 and c-Myc alone. These results suggested that KLF8 might be a weak oncogene that works cooperatively with c-Myc to transform ovarian cells. Surprisingly, overexpression of KLF8 alone was sufficient to induce tumorigenesis in nude mice resulting in short lifespan irrespective of whether the T80/KLF8 cells were injected subcutaneously, intraperitoneally or orthotopically into the ovarian bursa. Histopathological studies confirmed that the T80/KLF8 tumors were characteristic of human serous ovarian carcinomas. Comparative expression profiling and functional studies identified the cell cycle regulators cyclin D1 and USP44 as primary KLF8 targets and effectors for the T80 transformation. Overall, we identified KLF8 overexpression as an important factor in human ovarian carcinoma pathogenesis.

Indexed as

AnimalsCell LineCell ProliferationCell Transformation, NeoplasticCyclin D1Epithelial CellsFemaleGene Expression Regulation, NeoplasticHumansKruppel-Like Transcription FactorsMiceMice, NudeNeoplasm TransplantationOvarian NeoplasmsOvaryRepressor ProteinsCCND1 protein, humanCyclin D1KLF8 protein, humanKruppel-Like Transcription FactorsRepressor ProteinsUbiquitin-Specific ProteasesUbiquitin ThiolesteraseUSP44 protein, human

Identifiers

PMID23222713
PMCPMC3975924
OpenAlexW1966103152

What OpenQuestion holds

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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.