Evidence map›Paper›PMID 25197077›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Phospholipase Cδ1 induces E-cadherin expression and suppresses malignancy in colorectal cancer cells.

Reiko Satow, Tamaki Hirano, Ryosuke Batori, Tomomi Nakamura, Yumi Murayama, Kiyoko Fukami

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  5. Article
  6. Molecular regulation of PLCβ signaling.Methods in enzymology · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Phospholipase C.Advances in experimental medicine and biology · 2020
    Review
  13. Frontiers in genetics · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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

6 authors at 2 institutions in 1 country.

Reiko SatowLaboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan; and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo 192-0392, Japan.
Tamaki HiranoLaboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan; and.
Ryosuke BatoriLaboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan; and.
Tomomi NakamuraLaboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan; and.
Yumi MurayamaLaboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan; and.
Kiyoko FukamiLaboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan; and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo 192-0392, Japan kfukami@toyaku.ac.jp.
Tokyo University of Pharmacy and Life Sciences · JPJapan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the most common causes of cancer-related deaths worldwide, and Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations in CRC predict the ineffectiveness of EGF receptor-targeted therapy. Previous transcriptional microarray analysis suggests the association between phospholipase Cδ1 (PLCδ1) expression and KRAS mutation status in CRC. However, both the roles and the regulatory mechanisms of PLCδ1 in CRC are not known. Here, we found that the expression of PLCδ1, one of the most basal PLCs, is down-regulated in CRC specimens compared with normal colon epithelium by immunohistochemistry. Furthermore, we examined the roles of PLCδ1 in CRC cell lines that harbor an activating KRAS mutation. Ectopic expression of PLCδ1 in CRC cells induced the expression of E-cadherin, whereas knockdown of PLCδ1 repressed the expression of E-cadherin. Moreover, the overexpression of PLCδ1 suppressed the expression of several mesenchymal genes and reduced cell motility, invasiveness, and in vivo tumorigenicity of SW620 CRC cells. We also showed that PLCδ1 expression is repressed by the KRAS/mitogen-activated protein kinase kinase (MEK) pathway. Furthermore, PLCδ1 suppressed the phosphorylation of extracellular signal-regulated kinase (ERK)1/2 through E-cadherin induction in CRC cells, suggesting the presence of a negative regulatory loop between KRAS/MEK/ERK signaling and PLCδ1. These data indicate that PLCδ1 has tumor-suppressive functions in CRC through E-cadherin induction and KRAS/MEK/ERK signal attenuation.

Indexed as

AdenocarcinomaAntigens, CDCadherinsCarcinogenesisCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsDown-RegulationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMitogen-Activated Protein Kinase KinasesNeoplasm InvasivenessPhenotypeAntigens, CDCadherinsCDH1 protein, humanMitogen-Activated Protein Kinase KinasesPhospholipase C deltaepithelial-to-mesenchymal transitionphospholipase C delta 1tumor suppressor

Identifiers

PMID25197077
PMCPMC4169964
OpenAlexW2038862795

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.