Evidence map›Paper›PMID 19930715›Full record

ArticleMolecular cancer2009

PRL-3 promotes the motility, invasion, and metastasis of LoVo colon cancer cells through PRL-3-integrin beta1-ERK1/2 and-MMP2 signaling.

Lirong Peng, Xiaofang Xing, Weijun Li, Like Qu, Lin Meng, Shenyi Lian, Beihai Jiang, Jian Wu, Chengchao Shou

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

56 citing papers in PubMed, 91 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

9 authors at 3 institutions in 2 countries.

Lirong PengKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Biochemistry and Molecular Biology, Peking University School of Oncology, Beijing Cancer Hospital & Institute, Beijing 100142, PR China. lrpeng@hotmail.com
Xiaofang Xing
Weijun Li
Like Qu
Lin Meng
Shenyi Lian
Beihai Jiang
Jian Wu
Chengchao Shou
Peking University Cancer Hospital · CNPeking University · CNMinistry of Education · ET

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPhosphatase of regenerating liver-3 (PRL-3) plays a causative role in tumor metastasis, but the underlying mechanisms are not well understood. In our previous study, we observed that PRL-3 could decrease tyrosine phosphorylation of integrin beta1 and enhance activation of ERK1/2 in HEK293 cells. Herein we aim to explore the association of PRL-3 with integrin beta1 signaling and its functional implications in motility, invasion, and metastasis of colon cancer cell LoVo.

methodsTranswell chamber assay and nude mouse model were used to study motility and invasion, and metastsis of LoVo colon cancer cells, respectively. Knockdown of integrin beta1 by siRNA or lentivirus were detected with Western blot and RT-PCR. The effect of PRL-3 on integrin beta1, ERK1/2, and MMPs that mediate motility, invasion, and metastasis were measured by Western blot, immunofluorencence, co-immunoprecipitation and zymographic assays.

resultsWe demonstrated that PRL-3 associated with integrin beta1 and its expression was positively correlated with ERK1/2 phosphorylation in colon cancer tissues. Depletion of integrin beta1 with siRNA, not only abrogated the activation of ERK1/2 stimulated by PRL-3, but also abolished PRL-3-induced motility and invasion of LoVo cells in vitro. Similarly, inhibition of ERK1/2 phosphorylation with U0126 or MMP activity with GM6001 also impaired PRL-3-induced invasion. In addition, PRL-3 promoted gelatinolytic activity of MMP2, and this stimulation correlated with decreased TIMP2 expression. Moreover, PRL-3-stimulated lung metastasis of LoVo cells in a nude mouse model was inhibited when integrin beta1 expression was interfered with shRNA.

conclusionOur results suggest that PRL-3's roles in motility, invasion, and metastasis in colon cancer are critically controlled by the integrin beta1-ERK1/2-MMP2 signaling.

Indexed as

Neoplasm InvasivenessNeoplasm MetastasisBlotting, WesternCell Line, TumorColonic NeoplasmsExtracellular Signal-Regulated MAP KinasesHumansImmunohistochemistryIntegrin beta1Matrix Metalloproteinase 2Neoplasm ProteinsPhosphorylationProtein Tyrosine PhosphatasesRNA InterferenceSignal TransductionExtracellular Signal-Regulated MAP KinasesIntegrin beta1Matrix Metalloproteinase 2Neoplasm ProteinsProtein Tyrosine PhosphatasesPTP4A3 protein, human

Identifiers

PMID19930715
PMCPMC2792223
OpenAlexW2150426114

What OpenQuestion holds

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Registered trials

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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.