Evidence map›Paper›PMID 26242263›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

CCL18 promotes the invasion and migration of gastric cancer cells via ERK1/2/NF-κB signaling pathway.

Xu Hou, Ying Zhang, Haiquan Qiao

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. CCL18 in the Progression of Cancer.International journal of molecular sciences · 2020
    Review
  9. Review
  10. Article
  11. The expression of CCL18 in diffuse large B cell lymphoma and its mechanism research.Cancer biomarkers : section A of Disease markers · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Review
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

3 authors at 2 institutions in 1 country.

Xu HouDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, #23 You Zheng Road, Harbin, 150001, Heilongjiang Province, China.
Ying ZhangDepartment of Geriatrics, The Heilongjiang Provincial Hospital, Harbin, 150001, Heilongjiang Province, China.
Haiquan QiaoDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, #23 You Zheng Road, Harbin, 150001, Heilongjiang Province, China. haiquanqiaovv@163.com.
Harbin Medical University · CNHeilongjiang Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCL18 is a member of CCL chemokines and is frequently overexpressed in cancer. Elevated CCL18 expression has been reported to be associated with poor prognosis of gastric cancer. However, the molecular mechanisms of CCL18 in gastric cancer cells remain elusive. In our study, we found that CCL18 was highly expressed in different gastric cancer cells. CCL18 stimulation dose-dependently enhanced the invasion and migration of MGC-803 cells. Knockdown of endogenous CCL18 inhibited the invasion and migration of MGC-803 cells, whereas overexpression of CCL18 promoted the invasion and migration of MKN28 cells. We further found that CCL18 increased the expressions of MMP-3 and Slug and decreased the expression of E-cadherin in MGC-803 cells. In addition, CCL18 time-dependently induced activation of ERK1/2, IκBα, and NF-κB. These effects of CCL18 were prevented by ERK1/2 selective inhibitor U0126 as well as NF-κB selective inhibitor BAY117082. Taken together, our findings establish a signaling role for CCL18 in gastric cancer cells and identify that the CCL18/ERK1/2/NF-κB signaling pathway is essential for tumor invasiveness in gastric cancer cells. Thus, our data may provide knowledge for using CCL18 as a novel target for effective diagnosis and treatment of gastric cancer.

Indexed as

Signal TransductionCadherinsCell Line, TumorCell MovementChemokines, CCGene ExpressionGene Expression Regulation, NeoplasticHumansMatrix Metalloproteinase 3Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BProtein Kinase InhibitorsSnail Family Transcription FactorsStomach NeoplasmsCadherinsCCL18 protein, humanChemokines, CCMatrix Metalloproteinase 3Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BProtein Kinase InhibitorsSNAI1 protein, humanSnail Family Transcription FactorsCCL18ERK1/2Gastric cancerInvasionMigrationNF-κB

Identifiers

PMID26242263
OpenAlexW2139898656

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.