Evidence map›Paper›PMID 36263432›Full record

ReviewFrontiers in genetics2022

Histone deacetylases modulate resistance to the therapy in lung cancer.

Estefanía Contreras-Sanzón, Heriberto Prado-Garcia, Susana Romero-Garcia, David Nuñez-Corona, Blanca Ortiz-Quintero, Cesar Luna-Rivero, Victor Martínez-Cruz, Ángeles Carlos-Reyes

Abstract readReview
In one paragraph

Review in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. [Potential Mechanisms and Research Advances of HDAC1 in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026
    Review
  2. Review
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  4. Clinical progress and functional modalities of HDAC inhibitor-based combination therapies in cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  5. Review
  6. Article
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  12. Review
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  15. Article
  16. Article
  17. Article
  18. Epigenetic regulation of pulmonary inflammation.Seminars in cell & developmental biology · 2024
    Review
  19. Article
  20. 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

8 authors.

Estefanía Contreras-SanzónPosgrado de Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Ciudad de México, México.
Heriberto Prado-GarciaLaboratorio de Onco-Inmunobiologia, Departamento de Enfermedades Crónico-Degenerativas, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Ciudad de México, México.
Susana Romero-GarciaFacultad de Ciencias, Universidad Nacional Autónoma de México, Ciudad de México, México.
David Nuñez-CoronaPosgrado de Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Ciudad de México, México.
Blanca Ortiz-QuinteroDepartamento de Investigación en Bioquímica, Unidad de Investigación, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Ciudad de México, México.
Cesar Luna-RiveroServicio de Patología, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Ciudad de México, México.
Victor Martínez-CruzLaboratorio de Biología Molecular, Instituto Nacional de Pediatría, Ciudad de México, México.
Ángeles Carlos-ReyesLaboratorio de Onco-Inmunobiologia, Departamento de Enfermedades Crónico-Degenerativas, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Ciudad de México, México.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The acetylation status of histones located in both oncogenes and tumor suppressor genes modulate cancer hallmarks. In lung cancer, changes in the acetylation status are associated with increased cell proliferation, tumor growth, migration, invasion, and metastasis. Histone deacetylases (HDACs) are a group of enzymes that take part in the elimination of acetyl groups from histones. Thus, HDACs regulate the acetylation status of histones. Although several therapies are available to treat lung cancer, many of these fail because of the development of tumor resistance. One mechanism of tumor resistance is the aberrant expression of HDACs. Specific anti-cancer therapies modulate HDACs expression, resulting in chromatin remodeling and epigenetic modification of the expression of a variety of genes. Thus, HDACs are promising therapeutic targets to improve the response to anti-cancer treatments. Besides, natural compounds such as phytochemicals have potent antioxidant and chemopreventive activities. Some of these compounds modulate the deregulated activity of HDACs (e.g. curcumin, apigenin, EGCG, resveratrol, and quercetin). These phytochemicals have been shown to inhibit some of the cancer hallmarks through HDAC modulation. The present review discusses the epigenetic mechanisms by which HDACs contribute to carcinogenesis and resistance of lung cancer cells to anticancer therapies.

Indexed as

HDACs inhibitorshistone deacetylases (HDACs)lung cancernatural compoundsresistance to therapy

Identifiers

PMID36263432
PMCPMC9574126

What OpenQuestion holds

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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.