Evidence map›Paper›PMID 20426790›Full record

ArticleCancer science2010

Phosphatidylinositol 4,5-bisphosphate and PIP5-kinase Ialpha are required for invadopodia formation in human breast cancer cells.

Hideki Yamaguchi, Shuhei Yoshida, Emi Muroi, Masahiro Kawamura, Zen Kouchi, Yoshikazu Nakamura, Ryuichi Sakai, Kiyoko Fukami

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-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

35 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
  5. PI(4,5)P2: signaling the plasma membrane.The Biochemical journal · 2022
    Article
  6. Article
  7. PI(3,4)PProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. Article
  9. Article
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  11. Article
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  13. Article
  14. A new front in cell invasion: The invadopodial membrane.European journal of cell biology · 2016
    Review
  15. Article
  16. Article
  17. The role of PI3K/AKT-related PIP5K1α and the discovery of its selective inhibitor for treatment of advanced prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 2 countries.

Hideki YamaguchiLaboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Shuhei Yoshida
Emi Muroi
Masahiro Kawamura
Zen Kouchi
Yoshikazu Nakamura
Ryuichi Sakai
Kiyoko Fukami
Tokyo University of Pharmacy and Life Sciences · JPNational Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invadopodia are ventral cell protrusions formed in invasive cancer cells. Because invadopodia have extracellular matrix (ECM) degradation activity, they are thought to function in cancer invasion. In this study, we examined the roles of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)] and PI(4,5)P(2)-producing enzymes in invadopodia formation in MDA-MB-231 human breast cancer cells. Immunofluorescence analysis showed that PI(4,5)P(2) accumulates at invadopodia on the ventral cell surface. Injection of an anti-PI(4,5)P(2) antibody inhibited invadopodia formation along with gelatin degradation activity. Sequestering of PI(4,5)P(2) by overexpression of the phospholipase C (PLC) delta1-pleckstrin homology (PH) domain, a specific probe for PI(4,5)P(2), also blocked invadopodia formation, while a mutated PLCdelta1-PH domain that lacks PI(4,5)P(2)-binding activity had no effect. Cellular PI(4,5)P(2) production is mainly mediated by type-I phosphatidylinositol 4-phosphate 5-kinase (PIP5KI) family proteins, which include PIP5KIalpha, Ibeta, and Igamma. Real-time quantitative PCR analysis showed that PIP5KIalpha is a dominant isoform expressed in MDA-MB-231 cells. Knockdown of PIP5KIalpha by small-interfering RNA (siRNA) inhibited invadopodia formation and gelatin degradation. Immunofluorescence analysis revealed that endogenous PIP5KIalpha protein localizes at invadopodia, which is corroborated by the observation that exogenously expressed green fluorescent protein (GFP)-fused PIP5KIalpha protein also accumulates at gelatin degradation sites. These results indicate that localized production of PI(4,5)P(2) by PIP5KIalpha is required for invadopodia formation and ECM degradation by human breast cancer cells.

Indexed as

Neoplasm InvasivenessBreast NeoplasmsCell LineDNA PrimersFemaleHumansKineticsPhenotypePhosphatidylinositol 4,5-DiphosphatePhosphotransferases (Alcohol Group Acceptor)PlasmidsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceTransfectionTumor Cells, Cultured1-phosphatidylinositol-4-phosphate 5-kinaseDNA PrimersPhosphatidylinositol 4,5-DiphosphatePhosphotransferases (Alcohol Group Acceptor)

Identifiers

PMID20426790
PMCPMC11158062
OpenAlexW2088671515

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.