Evidence map›Paper›PMID 24168184›Full record

ReviewCurrent cancer drug targets2013

Regulation of EMT by KLF4 in gastrointestinal cancer.

Jiujie Cui, Min Shi, Ming Quan, Keping Xie

Open access · bronzeAbstract readReview
In one paragraph

Review in Current cancer drug targets, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Myeloid-derived suppressor cells modulation in the context of tumor microenvironment for gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. SIRT2-KLF4 Interactions are Critical for Myeloma Survival and Migration.Computational intelligence and neuroscience · 2022
    Article
  17. Article
  18. The Partial Role of KLF4 and KLF5 in Gastrointestinal Tumors.Gastroenterology research and practice · 2021
    Review
  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

4 authors at 2 institutions in 2 countries.

Jiujie Cui
Min Shi
Ming Quan
Keping XieDepartment of Gastroenterology, Hepatology & Nutrition, Unit 1466, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. kepxie@mdanderson.org.
Shanghai Jiao Tong University · CNThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Molecular Mediators of Pancreatic Cancer Invasion and ProgressionR01CA172233 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BRESALIER, ROBERT S · 2013 to 2017
$1.7M
Functional Validation of Pancreatic Cancer Progression BiomarkerR01CA152309 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2010 to 2014
$1.6M
KLF4 Genetic and Epigenetic Changes in Human Pancreatic CancerR01CA129956 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2008 to 2012
$1.3M
Genetic Approaches to Pancreatic Cancer ProgressionR01CA148954 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2010 to 2014
$1.3M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA129956NCI NIH HHS R01-CA129956NCI NIH HHS R01 CA148954NCI NIH HHS R01-CA148954NCI NIH HHS R01 CA152309NCI NIH HHS R01CA152309NCI NIH HHS R01 CA172233NCI NIH HHS R01CA172233
6 · The paper itself

Abstract

Gastrointestinal (GI) cancer is characterized by its aggressiveness, but the underlying mechanism is not fully understood. Studies reveal that epithelial to mesenchymal transition (EMT), which is regulated by a series of transcription factors and signaling pathways, is strongly associated with GI cancer cell proliferation, invasion and metastasis. Importantly, EMT is a product of crosstalk between signaling pathways. Krüppel-like factor 4 (KLF4), a zinc finger-type transcription factor, is decreased or lost in most GI cancers. By transcriptionally regulating its downstream target genes, KLF4 plays important roles of GI cancer tumorigenesis, proliferation and differentiation. In this review, we focus on the mechanism of KLF4 in GI cancer EMT, and demonstrate that through crosstalk with TGF-β, Notch, and Wnt signaling pathways, KLF4 negatively regulates EMT of GI cancers. Finally, we indicate the challenging new frontiers for KLF4 which contributes to better understanding of the mechanism of GI cancer aggressiveness.

Indexed as

AnimalsCarcinogenesisEpithelial-Mesenchymal TransitionGastrointestinal NeoplasmsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsSignal TransductionKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription Factors

Identifiers

PMID24168184
PMCPMC4127075
OpenAlexW2118956556

What OpenQuestion holds

Textmetadata
LicenceTDM
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.