Evidence map›Paper›PMID 26418031›Full record

ArticlePloS one2015

LPA Induces Colon Cancer Cell Proliferation through a Cooperation between the ROCK and STAT-3 Pathways.

Fernanda Leve, Rubem J Peres-Moreira, Renata Binato, Eliana Abdelhay, José A Morgado-Díaz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

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  5. Male-Biased Gut Microbiome and Metabolites Aggravate Colorectal Cancer Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
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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

5 authors at 2 institutions in 1 country.

Fernanda LeveDiretoria de Metrologia Aplicada às Ciências da Vida-Dimav, Instituto Nacional de Metrologia, Qualidade e Tecnologia-INMETRO, Xerém, Duque de Caxias, RJ, Brasil.
Rubem J Peres-MoreiraGrupo de Biologia Estrutural, Divisão de Biologia Celular, Centro de Pesquisas, Instituto Nacional de Câncer-INCA, Rio de Janeiro, RJ, Brasil.
Renata BinatoCentro de Transplante de Medula Óssea (CEMO), Instituto Nacional de Câncer-INCA, Rio de Janeiro, RJ, Brasil.
Eliana AbdelhayCentro de Transplante de Medula Óssea (CEMO), Instituto Nacional de Câncer-INCA, Rio de Janeiro, RJ, Brasil.
José A Morgado-DíazGrupo de Biologia Estrutural, Divisão de Biologia Celular, Centro de Pesquisas, Instituto Nacional de Câncer-INCA, Rio de Janeiro, RJ, Brasil.
Instituto Nacional do Câncer · BRInstituto Nacional de Metrologia, Qualidade e Tecnologia · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysophosphatidic acid (LPA) plays a critical role in the proliferation and migration of colon cancer cells; however, the downstream signaling events underlying these processes remain poorly characterized. The aim of this study was to investigate the signaling pathways triggered by LPA to regulate the mechanisms involved in the progression of colorectal cancer (CRC). We have used three cell line models of CRC, and initially analyzed the expression profile of LPA receptors (LPAR). Then, we treated the cells with LPA and events related to their tumorigenic potential, such as migration, invasion, anchorage-independent growth, proliferation as well as apoptosis and cell cycle were evaluated. We used the Chip array technique to analyze the global gene expression profiling that occurs after LPA treatment, and we identified cell signaling pathways related to the cell cycle. The inhibition of these pathways verified the conclusions of the transcriptomic analysis. We found that the cell lines expressed LPAR1, -2 and -3 in a differential manner and that 10 μM LPA did not affect cell migration, invasion and anchorage-independent growth, but it did induce proliferation and cell cycle progression in HCT-116 cells. Although LPA in this concentration did not induce transcriptional activity of β-catenin, it promoted the activation of Rho and STAT-3. Moreover, ROCK and STAT-3 inhibitors prevented LPA-induced proliferation, but ROCK inhibition did not prevent STAT-3 activation. Finally, we observed that LPA regulates the expression of genes related to the cell cycle and that the combined inhibition of ROCK and STAT-3 prevented cell cycle progression and increased the LPA-induced expression of cyclins E1, A2 and B1 to a greater degree than either inhibitor alone. Overall, these results demonstrate that LPA increases the proliferative potential of colon adenocarcinoma HCT-116 cells through a mechanism involving cooperation between the Rho-ROCK and STAT3 pathways involved in cell cycle control.

Indexed as

Apoptosisbeta CateninBlotting, WesternCell CycleCell MovementCell ProliferationColonic NeoplasmsFluorescent Antibody TechniqueHumansLysophospholipidsPhosphorylationReceptors, Lysophosphatidic Acidrho-Associated KinasesSignal TransductionSTAT3 Transcription FactorTumor Cells, Culturedbeta Cateninlysophosphatidic acidLysophospholipidsReceptors, Lysophosphatidic Acidrho-Associated KinasesSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID26418031
PMCPMC4587977
OpenAlexW2259367957

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.