Evidence map›Paper›PMID 34600336›Full record

ArticleRedox biology2021

HDAC inhibition induces EMT and alterations in cellular iron homeostasis to augment ferroptosis sensitivity in SW13 cells.

Thais Oliveira, Evan Hermann, Daniel Lin, Winyoo Chowanadisai, Elizabeth Hull, McKale Montgomery

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

53 citing papers in PubMed, 79 citations in OpenAlex.

  1. PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026
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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

6 authors at 2 institutions in 1 country.

Thais OliveiraDepartment of Nutritional Sciences, Oklahoma State University, Stillwater, OK, 74074, USA. Electronic address: thais.g.oliveira@okstate.edu.
Evan HermannDepartment of Nutritional Sciences, Oklahoma State University, Stillwater, OK, 74074, USA. Electronic address: evanhermann93@gmail.com.
Daniel LinDepartment of Nutritional Sciences, Oklahoma State University, Stillwater, OK, 74074, USA. Electronic address: dingbo.lin@okstate.edu.
Winyoo ChowanadisaiDepartment of Nutritional Sciences, Oklahoma State University, Stillwater, OK, 74074, USA. Electronic address: winyoo.chowanadisai@okstate.edu.
Elizabeth HullBiomedical Sciences, Midwestern University, Glendale, AZ, 85308, USA. Electronic address: ehullx@midwestern.edu.
McKale MontgomeryDepartment of Nutritional Sciences, Oklahoma State University, Stillwater, OK, 74074, USA. Electronic address: mckale.montgomery@okstate.edu.
Oklahoma State University · USMidwestern University · US

Funding

Impact of P53 Mutations on Cancer Cell Iron MetabolismR03CA241876 · NCI · OKLAHOMA STATE UNIVERSITY STILLWATER · PI MONTGOMERY, MCKALE · 2020 to 2020
$145k
NCI NIH HHS R03 CA241876
6 · The paper itself

Abstract

Epithelial-to-mesenchymal transition (EMT) is an essential mechanism for development and wound healing, but in cancer it also mediates the progression and spread of aggressive tumors while increasing therapeutic resistance. Adoption of a mesenchymal state is also associated with increased iron uptake, but the relationship between EMT and the key regulators of cellular iron metabolism remains undefined. In this regard, the human adrenal cortical carcinoma SW13 cell line represents an invaluable research model as HDAC inhibitor treatment can convert them from an epithelial-like (SW13-) cell type to a mesenchymal-like (SW13+) subtype. In this study we establish SW13 cells as a model for exploring the link between iron and EMT. Increased iron accumulation following HDAC inhibitor mediated EMT is associated with decreased expression of the iron export protein ferroportin, enhanced ROS production, and reduced expression of antioxidant response genes. As availability of redox active iron and loss of lipid peroxide repair capacity are hallmarks of ferroptosis, a form of iron-mediated cell death, we next examined whether HDAC inhibitor treatment could augment ferroptosis sensitivity. Indeed, HDAC inhibitor treatment synergistically increased cell death following induction of ferroptosis. The exact mechanisms by which HDAC inhibition facilitates cell death following ferroptosis induction requires further study. As several HDAC inhibitors are already in use clinically for the treatment of certain cancer types, the findings from these studies have immediate implications for improving iron-targeted chemotherapeutic strategies.

Indexed as

FerroptosisCell Line, TumorEpithelial-Mesenchymal TransitionHistone Deacetylase InhibitorsHomeostasisHumansIronHistone Deacetylase InhibitorsIronEpithelial-to-mesenchymal transition (EMT)FerroptosisHistone deacetylase (HDAC) inhibitorsIron

Identifiers

PMID34600336
PMCPMC8487084
OpenAlexW3202474249

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.