Evidence map›Paper›PMID 25081533›Full record

ReviewAdvances in cancer research2014

Hyaluronan-CD44 interaction promotes oncogenic signaling, microRNA functions, chemoresistance, and radiation resistance in cancer stem cells leading to tumor progression.

Lilly Y W Bourguignon, Marisa Shiina, Jian-Jian Li

Open access · greenAbstract readReview
In one paragraph

Review in Advances in cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
24.1field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 129 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The Hyaluronan/CD44 Axis: A Double-Edged Sword in Cancer.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

20 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Lilly Y W BourguignonDepartment of Medicine, University of California at San Francisco & Endocrine Unit (111N), VA Medical Center, San Francisco, California, USA. Electronic address: lilly.bourguignon@ucsf.edu.
Marisa ShiinaDepartment of Medicine, University of California at San Francisco & Endocrine Unit (111N), VA Medical Center, San Francisco, California, USA.
Jian-Jian LiDepartment of Radiation Oncology, University of California Davis, Sacramento, California, USA.
San Francisco VA Medical Center · USUniversity of California, Davis · US

Funding

CD44/VARIANT CYTOSKELETON IN BREAST CANCER PROGRESSIONR01CA066163 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BOURGUIGNON, LILLY YW · 1995 to 2010
$2.6M
BLRD VA I01 BX000628NCI NIH HHS R01 CA066163NCI NIH HHS R01 CA66163RRD VA I01 RX000601
6 · The paper itself

Abstract

Hyaluronan (HA), a major component of the extracellular matrix (ECM), is enriched in many types of tumors. There is good evidence linking high levels of HA production in human carcinomas to an aggressive phenotype and tumor metastasis. HA is generally bound to CD44 isoforms (so-called CD44s and CD44v3) which are ubiquitous, abundant, and functionally important cell surface receptors. This chapter describes the evidence for HA/CD44v3-mediated activation of the cytoskeleton (e.g., ankyrin and GTPases) and matrix metalloproteinase (MMP) signaling during tumor progression. A special focus is placed on the role of HA-CD44v3 interaction in cancer stem cells (CSCs). Matrix HA is known to be present in CSC niches. Since CD44v3 serves as a CSC marker, it provides an important physical linkage between matrix HA and various transcription factors that regulate tumor cell functions through distinct signaling pathways. CSCs are known to be chemoresistant and/or radiation resistant and to cause cancer relapse. The purpose of this chapter is to review the most current research on the cellular and molecular biology of CSCs. The emphasis will be placed on both CSC niche and matrix HA-induced microRNA signaling plus various CSC functions (e.g., self-renewal, differentiation, and chemoresistance) during cancer progression. Understanding the regulation of CSCs is critically important for designing CSC-specific therapeutic targets to prevent cancer development and progression.

Indexed as

Drug Resistance, NeoplasmAnimalsAnkyrinsApoptosisCell MovementCell ProliferationCell SurvivalCytoskeletonDisease ProgressionHumansHyaluronan ReceptorsHyaluronic AcidMiceMicroRNAsNeoplasm InvasivenessNeoplasmsAnkyrinsCD44 protein, humanHyaluronan ReceptorsHyaluronic AcidMicroRNAsrho GTP-Binding ProteinsCancer stem cellsCD44ChemoresistanceMatrix hyaluronanmicroRNAsRadiation resistanceTumor progression

Identifiers

PMID25081533
PMCPMC6759082
OpenAlexW1517984188

What OpenQuestion holds

Textmetadata
LicenceTDM
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.