Evidence map›Paper›PMID 20726856›Full record

ArticleCancer science2010

Spliceostatin A blocks angiogenesis by inhibiting global gene expression including VEGF.

Ryohei Furumai, Kazuyo Uchida, Yusuke Komi, Misao Yoneyama, Ken Ishigami, Hidenori Watanabe, Soichi Kojima, Minoru Yoshida

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
2.3field-weighted citation impact, top 12% 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, 57 citations in OpenAlex.

  1. Review
  2. Review
  3. Research progress and therapeutic prospect of PHF5A acting as a new target for malignant tumors.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Review
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  7. Review
  8. Review
  9. Article
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  13. Article
  14. Alternative splicing in prostate cancer.Nature reviews. Clinical oncology · 2018
    Review
  15. Article
  16. Review
  17. Article
  18. Article
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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

8 authors at 4 institutions in 2 countries.

Ryohei FurumaiChemical Genetics Laboratory Molecular Ligand Biology Research Team, Chemical Genomics Research Group, RIKEN Advanced Science Institute, Wako, Saitama, Japan.
Kazuyo Uchida
Yusuke Komi
Misao Yoneyama
Ken Ishigami
Hidenori Watanabe
Soichi Kojima
Minoru Yoshida
RIKEN Advanced Science Institute · JPLaboratory of Molecular Genetics · PLThe University of Tokyo · JPJapan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spliceostatin A (SSA) is a methylated derivative of an antitumor natural product FR901464, which specifically binds and inhibits the SF3b spliceosome sub-complex. To investigate the selective antitumor activity of SSA, we focused on the regulation of vascular endothelial growth factor (VEGF) mRNA, since VEGF is a key regulatory component in tumor angiogenesis and known for the intricate regulation of mRNA processing, such as alternative splicing. We found that in HeLa cells SSA reduced the amount of both mRNA and protein of VEGF. Spliceostatin A not only inhibited the splicing reaction of VEGF pre-mRNA but also reduced the total amount of VEGF's transcripts, while SSA affected GAPDH mRNA to a lesser extent. Given a significant reduction in VEGF gene expression, SSA was expected to possess anti-angiogenic activity in vivo. Indeed, SSA inhibited cancer cell-derived angiogenesis in vivo in a chicken chorioallantoic membrane (CAM) assay. The inhibition of angiogenesis with SSA was abolished by addition of exogenous VEGF. We also performed global gene expression analyses of HeLa cells and found that the expression levels of 38% of total genes including VEGF decreased to <50% of the basal levels following 16 h of SSA treatment. These results suggest that the global interference of gene expression including VEGF in tumor cells is at least one of the mechanisms by which SSA (or FR901464) exhibits its strong antitumor activity.

Indexed as

Angiogenesis InhibitorsAnimalsBlotting, WesternChick EmbryoChorioallantoic MembraneDose-Response Relationship, DrugGene Expression Regulation, NeoplasticHeLa CellsHumansMolecular StructureNeovascularization, PathologicOligonucleotide Array Sequence AnalysisPyransReverse Transcriptase Polymerase Chain ReactionSpiro CompoundsVascular Endothelial Growth Factor AAngiogenesis InhibitorsPyransSpiro Compoundsspliceostatin AVascular Endothelial Growth Factor A

Identifiers

PMID20726856
PMCPMC11158552
OpenAlexW1984059453

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.