Evidence map›Paper›PMID 25605242›Full record

ArticleOncotarget2015

Slit2/Robo1 signaling promotes intestinal tumorigenesis through Src-mediated activation of the Wnt/β-catenin pathway.

Qian-Qian Zhang, Da-Lei Zhou, Yan Lei, Li Zheng, Sheng-Xia Chen, Hong-Ju Gou, Qu-Liang Gu, Xiao-Dong He, Tian Lan, Cui-Ling Qi and 4 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 22% 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

30 citing papers in PubMed, 41 citations in OpenAlex.

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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

14 authors at 4 institutions in 2 countries.

Qian-Qian ZhangVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Da-Lei ZhouVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Yan LeiVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Li ZhengVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Sheng-Xia ChenVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Hong-Ju GouDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Qu-Liang GuVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Xiao-Dong HeVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Tian LanVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Cui-Ling QiVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Jiang-Chao LiVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Yan-Qing DingDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Liang QiaoStorr Liver Center, Westmead Millennium Institute for Medical Research, The Western Clinical School of the Faculty of Medicine, The University of Sydney at the Westmead Hospital, Westmead, NSW, Australia.
Li-Jing WangVascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, China.
Guangdong Pharmaceutical University · CNNanfang Hospital · CNSouthern Medical University · CNWestmead Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Slit2 is often overexpressed in cancers. Slit2 is a secreted protein that binds to Roundabout (Robo) receptors to regulate cell growth and migration. Here, we employed several complementary mouse models of intestinal cancers, including the Slit2 transgenic mice, the ApcMin/+ spontaneous intestinal adenoma mouse model, and the DMH/DSS-induced colorectal carcinoma model to clarify function of Slit2/Robo1 signaling in intestinal tumorigenesis. We showed that Slit2 and Robo1 are overexpressed in intestinal tumors and may contribute to tumor generation. The Slit2/Robo1 signaling can induce precancerous lesions of the intestine and tumor progression. Ectopic expression of Slit2 activated Slit2/Robo1 signaling and promoted tumorigenesis and tumor growth. This was mediated in part through activation of the Src signaling, which then down-regulated E-cadherin, thereby activating Wnt/β-catenin signaling. Thus, Slit2/Robo1 signaling is oncogenic in intestinal tumorigenesis.

Indexed as

Wnt Signaling PathwayAdenomaAnimalsbeta CateninCarcinomaCell ProliferationCell Transformation, NeoplasticColorectal NeoplasmsDisease Models, AnimalDisease ProgressionFemaleGenes, APCHCT116 CellsHumansIntercellular Signaling Peptides and ProteinsIntestinal Mucosabeta CateninCTNNB1 protein, humanCTNNB1 protein, mouseIntercellular Signaling Peptides and ProteinsNerve Tissue ProteinsReceptors, ImmunologicRoundabout ProteinsSlit Homolog 2 Proteinsrc-Family Kinases

Identifiers

PMID25605242
PMCPMC4413642
OpenAlexW1876256408

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.