Evidence map›Paper›PMID 18317448›Full record

ReviewOncogene2008

Autocrine induction of invasion and metastasis by tumor-associated trypsin inhibitor in human colon cancer cells.

V Gouyer, D Fontaine, P Dumont, O de Wever, H Fontayne-Devaud, E Leteurtre, S Truant, D Delacour, H Drobecq, J-P Kerckaert and 5 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-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

29 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Functional Roles of SPINK1 in Cancers.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. A novel discriminant score based on tumor-associated trypsin inhibitor for accurate diagnosis of metastasis in patients with breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  15. Colon cancer cells escape 5FU chemotherapy-induced cell death by entering stemness and quiescence associated with the c-Yes/YAP axis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Article
  16. Human colonic crypts in culture: segregation of immunochemical markers in normal versus adenoma-derived.Laboratory investigation; a journal of technical methods and pathology · 2014
    Article
  17. Article
  18. Article
  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

15 authors at 6 institutions in 3 countries.

V GouyerCentre de Recherche Jean-Pierre Aubert, U837, Faculté de Médecine, Lille, France.
D Fontaine
P Dumont
O de Wever
H Fontayne-Devaud
E Leteurtre
S Truant
D Delacour
H Drobecq
J-P Kerckaert
Y de Launoit
M Bracke
C Gespach
J-L Desseyn
G Huet
Centre de Recherche Jean Pierre Aubert · FRCentre Hospitalier Universitaire de Lille · FRInstitut de Biologie de Lille · FRGhent University Hospital · BEInserm · FRPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

From the conditioned medium of the human colon carcinoma cells, HT-29 5M21 (CM-5M21), expressing a spontaneous invasive phenotype, tumor-associated trypsin inhibitor (TATI) was identified and characterized by proteomics, cDNA microarray approaches and functional analyses. Both CM-5M21 and recombinant TATI, but not the K18Y-TATI mutant at the protease inhibitor site, trigger collagen type I invasion by several human adenoma and carcinoma cells of the colon and breast, through phosphoinositide-3-kinase, protein kinase C and Rho-GTPases/Rho kinase-dependent pathways. Conversely, the proinvasive action of TATI in parental HT29 cells was alleviated by the TATI antibody PSKAN2 and the K18Y-TATI mutant. Stable expression of K18Y-TATI in HT-29 5M21 cells downregulated tumor growth, angiogenesis and the expression of several metastasis-related genes, including CSPG4 (13.8-fold), BMP-7 (9.7-fold), the BMP antagonist CHORDIN (5.2-fold), IGFBP-2 and IGF2 (9.6- and 4.6-fold). Accordingly, ectopic expression of KY-TATI inhibited the development of lung metastases from HT-29 5M21 tumor xenografts in immunodeficient mice. These findings identify TATI as an autocrine transforming factor potentially involved in early and late events of colon cancer progression, including local invasion of the primary tumor and its metastatic spread. Targeting TATI, its molecular partners and effectors may bring novel therapeutic applications for high-grade human solid tumors in the digestive and urogenital systems.

Indexed as

Autocrine CommunicationAdenomaAnimalsAntibodies, NeoplasmBreast NeoplasmsCell Line, TumorColonic NeoplasmsGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceMice, SCIDNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsNeovascularization, PathologicAntibodies, NeoplasmNeoplasm ProteinsRecombinant ProteinsTrypsin Inhibitor, Kazal Pancreatic

Identifiers

PMID18317448
OpenAlexW2089097320

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.