Evidence map›Paper›PMID 25381815›Full record

ArticleOncogene2015

FOXC2 promotes colorectal cancer metastasis by directly targeting MET.

Y-M Cui, H-L Jiao, Y-P Ye, C-M Chen, J-X Wang, N Tang, T-T Li, J Lin, L Qi, P Wu and 6 more

RetractedOpen access · bronzeAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

52 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Super-enhancer Acquisition Drives FOXC2 Expression in Middle Ear Cholesteatoma.Journal of the Association for Research in Otolaryngology : JARO · 2021
    Article
  12. Review
  13. Review
  14. Frontiers in cell and developmental biology · 2021
    Article
  15. Review
  16. Article
  17. CREB5 promotes invasiveness and metastasis in colorectal cancer by directly activating MET.Journal of experimental & clinical cancer research : CR · 2020
    Article
  18. International journal of molecular sciences · 2020
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 1 country.

Y-M Cui1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
H-L Jiao1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Y-P Ye1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
C-M Chen1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
J-X Wang1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
N Tang1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
T-T Li1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
J Lin1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
L Qi1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
P Wu1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
S-Y Wang1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
M-R HeGuangdong Provincial Key Laboratory of Gastroenterology and Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
L Liang1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
X-W BianInstitute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
W-T Liao1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Y-Q Ding1] Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [3] Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, Guangzhou, China.
Nanfang Hospital · CNSouthern Medical University · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is the major cause of death in colorectal cancer (CRC). Although multiple genes have been identified to be responsible for the development of CRC, the molecular changes that enable CRC cells to undergo early local invasion and to form distant metastatic colonies still remain largely unknown. Herein, we investigated the role of Forkhead box protein C2 (FOXC2) and explored the underlying mechanisms in invasion and metastasis of CRC. We show that both high FOXC2 expression and nuclear localization of FOXC2 are significantly correlated with advanced TNM (T=primary tumor; N=regional lymph nodes; M=distant metastasis) stages. FOXC2 enhanced the invasive abilities of CRC cells in vitro and promoted local invasion and distant metastasis in an orthotopic mouse metastatic model of CRC. Microarray analysis revealed that overexpression of FOXC2 increased the proto-oncogene MET tyrosine kinase expression and activated the hepatocyte growth factor (HGF)-MET signaling pathway. Furthermore, luciferase reporter assays and chromatin immunoprecipitation assays revealed that FOXC2 directly associated with MET promoter to increase the transcriptional activity of MET. Inhibition of MET attenuates the invasive phenotype and metastatic potential of FOXC2-overexpressing CRC cells, indicating that MET is a major mediator of FOXC2-promoted metastasis. In addition, FOXC2 expression was positively correlated with MET expression in CRC tissue samples. Our findings suggest that FOXC2 has a crucial role in CRC metastasis by regulating HGF-MET signaling via inducing MET expression, highlighting FOXC2 as a potential therapeutic target for preventing or reducing metastasis in CRC.

Indexed as

AnimalsCell Line, TumorCell MovementColorectal NeoplasmsForkhead Transcription FactorsGene Expression Regulation, NeoplasticHepatocyte Growth FactorHumansMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessNeoplasm MetastasisProto-Oncogene MasProto-Oncogene Proteins c-metSignal TransductionForkhead Transcription FactorsHepatocyte Growth FactorMAS1 protein, humanmesenchyme fork head 1 proteinProto-Oncogene MasProto-Oncogene Proteins c-met

Identifiers

PMID25381815
OpenAlexW2067057174

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.