Evidence map›Paper›PMID 33199827›Full record

ArticleOncogene2021

HDAC6 promotes growth, migration/invasion, and self-renewal of rhabdomyosarcoma.

Thao Q Pham, Kristin Robinson, Lin Xu, Maria N Pavlova, Stephen X Skapek, Eleanor Y Chen

Abstract read
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026
    Review
  2. Article
  3. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. HDAC6: A unique HDAC family member as a cancer target.Cellular oncology (Dordrecht, Netherlands) · 2022
    Review
  20. Targeting HDAC6 to Overcome Autophagy-Promoted Anti-Cancer Drug Resistance.International journal of molecular sciences · 2022
    Review
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.

Thao Q Pham *Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Kristin Robinson *Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Lin XuDepartment of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Maria N PavlovaDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Stephen X SkapekDepartment of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Eleanor Y ChenDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA. eleanor2@uw.edu.ORCID http://orcid.org/0000-0003-4372-7560

Funding

Characterizing Histone Deacetylases in RhabdomyosarcomaR01CA196882 · NCI · UNIVERSITY OF WASHINGTON · PI CHEN, ELEANOR Y · 2016 to 2020
$1.6M
NCI NIH HHS R01 CA196882
6 · The paper itself

Abstract

Rhabdomyosarcoma (RMS) is a devastating pediatric sarcoma. The survival outcomes remain poor for patients with relapsed or metastatic disease. Effective targeted therapy is lacking due to our limited knowledge of the underlying cellular and molecular mechanisms leading to disease progression. In this study, we used functional assays in vitro and in vivo (zebrafish and xenograft mouse models) to demonstrate the crucial role of HDAC6, a cytoplasmic histone deacetylase, in driving RMS tumor growth, self-renewal, and migration/invasion. Treatment with HDAC6-selective inhibitors recapitulates the HDAC6 loss-of-function phenotypes. HDAC6 regulates cytoskeletal dynamics to promote tumor cell migration and invasion. RAC1, a Rho family GTPase, is an essential mediator of HDAC6 function, and is necessary and sufficient for RMS cell migration and invasion. High expression of RAC1 correlates with poor clinical prognosis in RMS patients. Targeting the HDAC6-RAC1 axis represents a promising therapeutic option for improving survival outcomes of RMS patients.

Indexed as

Cell MovementCell ProliferationCell Line, TumorHistone Deacetylase 6HumansNeoplasm InvasivenessNeoplasm ProteinsRhabdomyosarcomaHDAC6 protein, humanHistone Deacetylase 6Neoplasm Proteins

Identifiers

PMID33199827
PMCPMC7855743

What OpenQuestion holds

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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.