Evidence map›Paper›PMID 24504172›Full record

ArticleOncotarget2014

Collagen triple helix repeat containing 1 (CTHRC1) acts via ERK-dependent induction of MMP9 to promote invasion of colorectal cancer cells.

Hee Cheol Kim, Yong Sung Kim, Hyun-Woo Oh, Kwoneel Kim, Sang-Seok Oh, Jong-Tae Kim, Bo Yeon Kim, Seon-Jin Lee, Yong-Kyung Choe, Dong Hyeok Kim and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. [Effects of RNA interference of CTHRC1 on proliferation and apoptosis of thyroid papillary cancer TCP-1 cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  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

14 authors at 3 institutions in 1 country.

Hee Cheol KimBiomedical Genomics Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, South Korea.
Yong Sung Kim
Hyun-Woo Oh
Kwoneel Kim
Sang-Seok Oh
Jong-Tae Kim
Bo Yeon Kim
Seon-Jin Lee
Yong-Kyung Choe
Dong Hyeok Kim
Seok-Hyung Kim
Seoung Wan Chae
Kwang Dong Kim
Hee Gu Lee
Korea Research Institute of Bioscience and Biotechnology · KRGyeongsang National University · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Collagen triple helix repeat-containing 1 (CTHRC1) is known to be aberrantly upregulated in most human solid tumors, although the functional roles of CTHRC1 in colorectal cancer remain unclear. In this study, we investigated the occurrence of CTHRC1 upregulation and its role in vivo and in vitro. The expression profile and clinical importance of CTHRC1 were examined by reverse transcription-polymerase chain reaction and immunohistochemical analyses in normal and tumor patient samples. CTHRC1 was detectable in normal tissues, but also was highly expressed in tumor specimens. CTHRC1 upregulation was significantly associated with demethylation of the CTHRC1 promoter in colon cancer cell lines and tumor tissues. Clinicopathologic analyses showed that nodal status and expression of CTHRC1 (95% CI 0.999-3.984, p=0.05) were significant prognostic factors for disease-free survival. Promoter CpG methylation and hypermethylation status were measured by bisulfite sequencing and pyrosequencing analysis. Furthermore, we showed that overexpression of CTHRC1 in the SW480 and HT-29 cell lines increased invasiveness, an effect mediated by extracellular signal-regulated kinase (ERK)-dependent upregulation of matrix metalloproteinase 9 (MMP9). Consistent with this, we found that knockdown of CTHRC1 attenuated ERK activation and cancer cell invasivity. These results demonstrate that CTHRC1 expression is elevated in human colon cancer cell lines and clinical specimens, and promotes cancer cell invasivity through ERK-dependent induction of MMP9 expression. Our results further suggest that high levels of CTHRC1 expression are associated with poor clinical outcomes.

Indexed as

AdenocarcinomaAdultAgedAged, 80 and overCell MovementColorectal NeoplasmsDisease-Free SurvivalEnzyme InductionExtracellular Matrix ProteinsExtracellular Signal-Regulated MAP KinasesFemaleHT29 CellsHumansMaleMatrix Metalloproteinase 9Middle AgedCTHRC1 protein, humanExtracellular Matrix ProteinsExtracellular Signal-Regulated MAP KinasesMatrix Metalloproteinase 9MMP9 protein, human

Identifiers

PMID24504172
PMCPMC3964226
OpenAlexW1501019277

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.