Evidence map›Paper›PMID 28970726›Full record

ArticleWorld journal of gastroenterology2017

Ca

Wei Chen, Ping An, Xiao-Jing Quan, Jun Zhang, Zhong-Yin Zhou, Li-Ping Zou, He-Sheng Luo

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Role of CaCancer medicine · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Effects and potential mechanism of CaInternational journal of molecular medicine · 2022
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. p21-Activated Kinase 1 Promotes Breast TumorigenesisFrontiers in cell and developmental biology · 2021
    Article
  18. CaJournal of cellular immunology · 2021
    Article
  19. Article
  20. 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

7 authors at 3 institutions in 2 countries.

Wei ChenDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Ping AnDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Xiao-Jing QuanDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Jun ZhangDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Zhong-Yin ZhouDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Li-Ping ZouDepartment of Education, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
He-Sheng LuoDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China. xhnk@163.com.
Harvard University · USRenmin Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the role of calmodulin-dependent protein kinase II (CaMKII) in colon cancer growth, migration and invasion.

methodsCaMKII expression in colon cancer and paracancerous tissues was evaluated via immunochemistry. Transcriptional and posttranscriptional levels of CaMKIIin tissue samples and MMP2, MMP9 and TIMP-1 expression in the human colon cancer cell line HCT116 were assessed by qRT-PCR and western blot. Cell proliferation was detected with the MTT assay. Cancer cell migration and invasion were investigated with the Transwell culture system and wound-healing assay.

resultsWe first demonstrated that CaMKII was over-expressed in human colon cancers and was associated with cancer differentiation. In the human colon cancer cell line HCT116, the CaMKII-specific inhibitor KN93, but not its inactive analogue KN92, decreased cancer cell proliferation. Furthermore, KN93 also significantly prohibited HCT116 cell migration and invasion. The specific inhibition of ERK1/2 or p38 decreased the proliferation and migration of colon cancer cells.

conclusionOur findings highlight CaMKII as a potential critical mediator in human colon tumor development and metastasis.

Indexed as

MAP Kinase Signaling SystemBenzenesulfonamidesBenzylaminesCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell DifferentiationCell Line, TumorCell MovementCell ProliferationColonic NeoplasmsHCT116 CellsHumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Neoplasm InvasivenessBenzenesulfonamidesBenzylaminesCalcium-Calmodulin-Dependent Protein Kinase Type 2CAMK2A protein, humanKN 92KN 93MAPK1 protein, humanMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MMP2 protein, humanMMP9 protein, humanp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsSulfonamidesTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1Ca2+/calmodulin-dependent protein kinase IIColon cancerMigrationProliferation

Identifiers

PMID28970726
PMCPMC5597502
OpenAlexW2755158403

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.