Evidence map›Paper›PMID 28319059›Full record

ArticleOncogene2017

CAMK2γ in intestinal epithelial cells modulates colitis-associated colorectal carcinogenesis via enhancing STAT3 activation.

X Ma, Z Meng, L Jin, Z Xiao, X Wang, W M Tsark, L Ding, Y Gu, J Zhang, B Kim and 6 more

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. CAMKIIδ Reinforces Lipid Metabolism and Promotes the Development of B Cell Lymphoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. MLKL inhibits intestinal tumorigenesis by suppressing STAT3 signaling pathway.International journal of biological sciences · 2021
    Article
  15. Review
  16. Review
  17. Endoplasmic Reticulum Stress/CaFrontiers in physiology · 2021
    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

16 authors at 4 institutions in 2 countries.

X MaMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
Z MengMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
L JinMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
Z XiaoMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
X WangMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
W M TsarkTransgenic Mouse Core, City of Hope National Medical Center, Duarte, CA, USA.
L DingMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
Y GuMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
J ZhangMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
B KimMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
M HeSchool of Public Health, Guangxi Medical University, Nanning, Guangxi, China.
X GanMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
J E ShivelyDepartments of Immunology, City of Hope National Medical Center, Duarte, CA, USA.
H YuDepartment of Cancer Immunotherapeutics and Tumor Immunology Beckman Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
R XuMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
W HuangMolecular and Cellular Biology of Cancer Program, Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA, USA.
City Of Hope National Medical Center · USZhejiang University · CNCleveland Clinic · USFujian Medical University · CN

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI XIWEI WU · 1985 to 2026
$86.3M
MiRNAs in hepatocellular carcinoma development and treatmentR01CA139158 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI HUANG, WENDONG, YU, HUA E · 2011 to 2021
$3.7M
NCI NIH HHS P30 CA033572NCI NIH HHS R01 CA139158
6 · The paper itself

Abstract

Inflammation is one of the major risk factors for cancer. Here, we show that calcium/calmodulin-dependent protein kinase II gamma (CAMK2γ) in intestinal epithelial cells (IECs) modulates inflammatory signals and promotes colitis-associated cancer (CAC) in mice. We have identified CAMK2γ as a downstream target of colitis-induced WNT5A signaling. Furthermore, we have shown that CAMK2γ protects against intestine tissue injury by increasing IEC survival and proliferation. Calcium/calmodulin-dependent protein kinase II gamma knockout mice displayed reduced CAC. Furthermore, we used bone marrow transplantation to reveal that CAMK2γ in IECs, but not immune cells, was crucial for its effect on CAC. Consistently, transgenic over-expression of CAMK2γ in IECs accelerated CAC development. Mechanistically, CAMK2γ in IECs enhanced epithelial signal transducer and activator of transcription 3 (STAT3) activation to promote survival and proliferation of colonic epithelial cells during CAC development. These results thus identify a new molecular mechanism mediated by CAMK2γ in IECs during CAC development, thereby providing a potential new therapeutic target for CAC.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2CarcinogenesisCell ProliferationColitisColorectal NeoplasmsEpithelial CellsHCT116 CellsHT29 CellsHumansIntestinal MucosaMiceMice, Inbred C57BLMice, KnockoutSTAT3 Transcription FactorCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2g protein, mouseSTAT3 Transcription Factor

Identifiers

PMID28319059
PMCPMC5509478
OpenAlexW2603530373

What OpenQuestion holds

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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.