Evidence map›Paper›PMID 35972597›Full record

ReviewMedical oncology (Northwood, London, England)2022

Differential molecular mechanistic behavior of HDACs in cancer progression.

Tashvinder Singh, Prabhsimran Kaur, Paramdeep Singh, Sandeep Singh, Anjana Munshi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Asiatic acid promotes CD8Acta pharmacologica Sinica · 2026
    Article
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  6. RNA 5-Methylcytosine Modification in Myocardial Fibrosis.Reviews in cardiovascular medicine · 2025
    Review
  7. Article
  8. Article
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  10. Uterine carcinosarcoma: Unraveling the role of epithelial-to-mesenchymal transition in progression and therapeutic potential.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Review
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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

5 authors at 1 institution in 1 country.

Tashvinder SinghDepartment of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151401, India.
Prabhsimran KaurDepartment of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151401, India.
Paramdeep SinghDepartment of Radiology, AIIMS, Bathinda, 151001, India.
Sandeep SinghDepartment of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151401, India. sandeepsingh82@cup.edu.in.ORCID http://orcid.org/0000-0001-8780-5124
Anjana MunshiDepartment of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151401, India. anjana.munshi@cup.edu.in.ORCID http://orcid.org/0000-0002-7657-8592
Central University of Punjab · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic aberration including mutation in oncogenes and tumor suppressor genes transforms normal cells into tumor cells. Epigenetic modifications work concertedly with genetic factors in controlling cancer development. Histone acetyltransferases (HATs), histone deacetylases (HDACs), DNA methyltransferases (DNMTs) and chromatin structure modifier are prospective epigenetic regulators. Specifically, HDACs are histone modifiers regulating the expression of genes implicated in cell survival, growth, apoptosis, and metabolism. The majority of HDACs are highly upregulated in cancer, whereas some have a varied function and expression in cancer progression. Distinct HDACs have a positive and negative role in controlling cancer progression. HDACs are also significantly involved in tumor cells acquiring metastatic and angiogenic potential in order to withstand the anti-tumor microenvironment. HDACs' role in modulating metabolic genes has also been associated with tumor development and survival. This review highlights and discusses the molecular mechanisms of HDACs by which they regulate cell survival, apoptosis, metastasis, invasion, stemness potential, angiogenesis, and epithelial to mesenchymal transitions (EMT) in tumor cells. HDACs are the potential target for anti-cancer drug development and various inhibitors have been developed and FDA approved for a variety of cancers. The primary HDAC inhibitors with proven anti-cancer efficacy have also been highlighted in this review.

Indexed as

Histone Deacetylase InhibitorsNeoplasmsHistone AcetyltransferasesHistone DeacetylasesHumansProspective StudiesTumor MicroenvironmentHistone AcetyltransferasesHistone Deacetylase InhibitorsHistone DeacetylasesAngiogenesisCancerHistone deacetylasesMetabolismMetastasisStemness potential

Identifiers

PMID35972597
OpenAlexW4291949328

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.