Evidence map›Paper›PMID 18320073›Full record

ArticleNeoplasia (New York, N.Y.)2008

Inhibition of JAK1, 2/STAT3 signaling induces apoptosis, cell cycle arrest, and reduces tumor cell invasion in colorectal cancer cells.

Hua Xiong, Zhi-Gang Zhang, Xiao-Qing Tian, Dan-Feng Sun, Qin-Chuan Liang, Yan-Jie Zhang, Rong Lu, Ying-Xuan Chen, Jing-Yuan Fang

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 2 pooled it
8.7field-weighted citation impact, top 2% 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

209 citing papers in PubMed, 2 syntheses or guidelines pooled it, 429 citations in OpenAlex.

  1. Genetic variants in IL-6/JAK/STAT3 pathway and the risk of CRC.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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149 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Hua XiongDepartment of Gastroenterology, Shanghai Jiao-Tong University School of Medicine, Ren-Ji Hospital, Shanghai Institute of Digestive Disease, Shanghai, 200001, China.
Zhi-Gang Zhang
Xiao-Qing Tian
Dan-Feng Sun
Qin-Chuan Liang
Yan-Jie Zhang
Rong Lu
Ying-Xuan Chen
Jing-Yuan Fang
Renji Hospital · CNShanghai Jiao Tong University · CNAir Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormalities in the STAT3 pathway are involved in the oncogenesis of several cancers. However, the mechanism by which dysregulated STAT3 signaling contributes to the progression of human colorectal cancer (CRC) has not been elucidated, nor has the role of JAK, the physiological activator of STAT3, been evaluated. To investigate the role of both JAK and STAT3 in CRC progression, we inhibited JAK with AG490 and depleted STAT3 with a SiRNA. Our results demonstrate that STAT3 and both JAK1 and 2 are involved in CRC cell growth, survival, invasion, and migration through regulation of gene expression, such as Bcl-2, p1(6ink4a), p21(waf1/cip1), p27(kip1), E-cadherin, VEGF, and MMPs. Importantly, the FAK is not required for STAT3-mediated regulation, but does function downstream of JAK. In addition, our data show that proteasome-mediated proteolysis promotes dephosphorylation of the JAK2, and consequently, negatively regulates STAT3 signaling in CRC. Moreover, immunohistochemical staining reveals that nuclear staining of phospho-STAT3 mostly presents in adenomas and adenocarcinomas, and a positive correlation is found between phospho-JAK2 immunoreactivity and the differentiation of colorectal adenocarcinomas. Therefore, our findings illustrate the biologic significance of JAK1, 2/STAT3 signaling in CRC progression and provide novel evidence that the JAK/STAT3 pathway may be a new potential target for therapy of CRC.

Indexed as

ApoptosisCadherinsCell CycleColorectal NeoplasmsCysteine Proteinase InhibitorsDown-RegulationFocal Adhesion Kinase 1HumansJanus Kinase 1Janus Kinase 2LeupeptinsMatrix Metalloproteinase 2Matrix Metalloproteinase 9Neoplasm InvasivenessProtein Kinase InhibitorsRNA, Small Interferingalpha-cyano-(3,4-dihydroxy)-N-benzylcinnamidebenzyloxycarbonylleucyl-leucyl-leucine aldehydeCadherinsCysteine Proteinase InhibitorsFocal Adhesion Kinase 1Janus Kinase 1Janus Kinase 2LeupeptinsMatrix Metalloproteinase 2Matrix Metalloproteinase 9Protein Kinase InhibitorsPTK2 protein, humanRNA, Small InterferingSTAT3 Transcription FactorTyrphostinsVascular Endothelial Growth Factor A

Identifiers

PMID18320073
PMCPMC2259457
OpenAlexW89255747

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.