Evidence map›Paper›PMID 26356816›Full record

ArticleOncotarget2015

C-kit signaling promotes proliferation and invasion of colorectal mucinous adenocarcinoma in a murine model.

Jun Tan, Shu Yang, Ping Shen, Haimei Sun, Jie Xiao, Yaxi Wang, Bo Wu, Fengqing Ji, Jihong Yan, Hong Xue and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  18. (+)-Usnic Acid Inhibits Migration of c-KIT Positive Cells in Human Colorectal Cancer.Evidence-based complementary and alternative medicine : eCAM · 2018
    Article
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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

11 authors at 1 institution in 1 country.

Jun TanDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Shu YangDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Ping ShenDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Haimei SunDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Jie XiaoDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Yaxi WangDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Bo WuDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Fengqing JiDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Jihong YanDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Hong XueDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Deshan ZhouDepartment of Histology and Embryology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P. R. China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It was reported that the receptor tyrosine kinase (RTK) family often highly expressed in several mucinous carcinomas. In the present study, we established a murine model of colorectal mucinous adenocardinoma (CRMAC) by treating C57 mice [both wild type (WT) and loss-of-function c-kit mutant type (Wads-/-)] with AOM+DSS for 37 weeks and found that c-kit, a member of RTK family, clearly enhanced the tumor cell proliferation by decreasing p53 and increasing cyclin D1 through AKT pathway. Significantly, c-kit strongly promoted tumor cell invasiveness by increasing ETV4, which induced MMP7 expression and epithelial-mesenchymal transition (EMT) via ERK pathway. In vitro up- or down-regulating c-kit activation in human colorectal cancer HCT-116 cells further consolidated these results. In conclusion, our data suggested that the c-kit signaling obviously promoted proliferation and invasion of CRMAC. Therefore, targeting the c-kit signaling and its downstream molecules might provide the potential strategies for treatment of patients suffering from CRMAC in the future.

Indexed as

AdenocarcinomaAdenocarcinoma, MucinousAnimalsCell Line, TumorCell ProliferationColorectal NeoplasmsCyclin D1Disease Models, AnimalEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticGenotypeHCT116 CellsHumansLentivirusMatrix Metalloproteinase 7AKT1 protein, humanAkt1 protein, mouseCCND1 protein, humanCcnd1 protein, mouseCyclin D1Extracellular Signal-Regulated MAP KinasesMatrix Metalloproteinase 7MMP7 protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-kitTP53 protein, humanTumor Suppressor Protein p53C-kitcolorectal mucinous adenocarcinomaETV4murine model

Identifiers

PMID26356816
PMCPMC4694972
OpenAlexW1824234743

What OpenQuestion holds

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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.