Evidence map›Paper›PMID 29356399›Full record

ArticleCancer medicine2018

SALL4 - KHDRBS3 network enhances stemness by modulating CD44 splicing in basal-like breast cancer.

Yoshiaki Matsumoto, Junji Itou, Fumiaki Sato, Masakazu Toi

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  13. SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. CD44 as a tumor biomarker and therapeutic target.Experimental hematology & oncology · 2020
    Review
  17. Article
  18. Knockdown ofAnnals of translational medicine · 2020
    Article
  19. Review
  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

4 authors at 1 institution in 1 country.

Yoshiaki MatsumotoDepartment of Breast Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-4256-2349
Junji ItouDepartment of Breast Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-0748-2327
Fumiaki SatoDepartment of Breast Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masakazu ToiDepartment of Breast Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the mechanism by which cancer cells enhance stemness facilitates cancer therapies. Here, we revealed that a stem cell transcription factor, SALL4, functions to enhance stemness in basal-like breast cancer cells. We used shRNA-mediated knockdown and gene overexpression systems to analyze gene functions. To evaluate stemness, we performed a sphere formation assay. In SALL4 knockdown cells, the sphere formation ability was reduced, indicating that SALL4 enhances stemness. CD44 is a membrane protein and is known as a stemness factor in cancer. CD44 splicing variants are involved in cancer stemness. We discovered that SALL4 modulates CD44 alternative splicing through the upregulation of KHDRBS3, a splicing factor for CD44. We cloned the KHDRBS3-regulated CD44 splicing isoform (CD44v), which lacks exons 8 and 9. CD44v overexpression prevented a reduction in the sphere formation ability by KHDRBS3 knockdown, indicating that CD44v is positively involved in cancer stemness. In addition, CD44v enhanced anoikis resistance under the control of the SALL4 - KHDRBS3 network. Basal-like breast cancer is an aggressive subtype among breast cancers, and there is no effective therapy so far. Our findings provide molecular targets for basal-like breast cancer therapy. In the future, this study may contribute to the establishment of drugs targeting cancer stemness.

Indexed as

Alternative SplicingBreast NeoplasmsFemaleHumansHyaluronan ReceptorsNeoplasms, Basal CellNeoplastic Stem CellsProtein IsoformsRNA-Binding ProteinsTranscription FactorsTumor Cells, CulturedCD44 protein, humanHyaluronan ReceptorsKHDRBS3 protein, humanProtein IsoformsRNA-Binding ProteinsSALL4 protein, humanTranscription FactorsBreast neoplasmsprotein isoformsRNA splicing factorsstem cell factortranscription factors

Identifiers

PMID29356399
PMCPMC5806117
OpenAlexW2791701000

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.