Evidence map›Paper›PMID 40550304›Full record

ArticleEnvironmental research2025

Chronic PFAS exposure induces chemotherapy resistance by promoting mitochondria-related alterations in ovarian cancer cells.

Brittany P Rickard, Lauren A Sapienza-Lundie, Marta Overchuk, Justin Tulino, Mateus Prates Mori, James P McCord, Vesna A Chappell, Carl D Bortner, Victoria L Bae-Jump, Janine H Santos and 2 more

Abstract read
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In one paragraph

Article in Environmental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
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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

12 authors.

Brittany P RickardDepartment of Biological Sciences, North Carolina State University, Raleigh, NC, 27606, USA; Curriculum in Toxicology & Environmental Medicine, University of North Carolina School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA; Lampe Joint Department of Biomedical Engineering University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 and North Carolina State University, Raleigh, NC, 27606, USA. Electronic address: bprickar@ncsu.edu.
Lauren A Sapienza-LundieCurriculum in Toxicology & Environmental Medicine, University of North Carolina School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA; Lampe Joint Department of Biomedical Engineering University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 and North Carolina State University, Raleigh, NC, 27606, USA.
Marta OverchukLampe Joint Department of Biomedical Engineering University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 and North Carolina State University, Raleigh, NC, 27606, USA.
Justin TulinoLampe Joint Department of Biomedical Engineering University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 and North Carolina State University, Raleigh, NC, 27606, USA.
Mateus Prates MoriMechanistic Toxicology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, 27709, USA.
James P McCordUS Environmental Protection Agency, Office of Research and Development, Center for Environmental Measurement and Modeling, Research Triangle Park, NC, 27711, USA.
Vesna A ChappellMechanistic Toxicology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, 27709, USA.
Carl D BortnerDivision of Intramural Research, National Institute of Environmental Health Sciences/NIH, Research Triangle Park, NC, 27709, USA.
Victoria L Bae-JumpDivision of Gynecologic Oncology, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA.
Janine H SantosMechanistic Toxicology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, 27709, USA.
Suzanne E FentonCenter for Human Health and the Environment, North Carolina State University, Raleigh, NC, 27606, USA.
Imran RizviCurriculum in Toxicology & Environmental Medicine, University of North Carolina School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA; Lampe Joint Department of Biomedical Engineering University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 and North Carolina State University, Raleigh, NC, 27606, USA; Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA; Center for Environmental Health and Susceptibility, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Hazel B Nichols · 2001 to 2026
$36.3M
Translational Research Support CoreP30ES025128 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Sue Fenton · 2015 to 2026
$18.3M
TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
Targeting Fluid Stress-induced Chemoresistance in a 3D Carcinomatosis Perfusion Model Using Mechanism-based Photo-immunoconjugate NanoparticlesR01CA256710 · NCI · UNIV OF MARYLAND, COLLEGE PARK · PI Huang Chiao Huang, Imran Rizvi · 2023 to 2026
$2.2M
Intramural EPA EPA999999NCI NIH HHS R01 CA256710NIEHS NIH HHS P30 ES010126NIEHS NIH HHS P30 ES025128NIEHS NIH HHS T32 ES007126
6 · The paper itself

Abstract

Resistance to chemotherapy is a major barrier to the effective treatment of ovarian cancer; however, the role of environmental exposures in the onset of chemoresistance remains elusive. Our previous work in ovarian cancer cells suggests that short-term perfluoroalkyl substances (PFAS) exposures induce chemoresistance, potentially by influencing mitochondrial parameters, but little is known about the effects of longer-term exposures, which are more human-relevant. Since mitochondria play critical roles in determining ovarian cancer chemotherapy response, it is also important to understand the role of environmental exposures in modulating mitochondrial function. This study explored how varying durations of PFAS exposure (2-35 days) affect mitochondrial parameters known to drive chemoresistance in human ovarian cancer cell lines. An ovarian cancer cell line (OVCAR-3) that was chronically exposed to PFAS (26-35 days) was generated. Compared to short-term PFAS exposure, chronic PFAS exposures significantly increased resistance to both carboplatin and doxorubicin. Chemotherapy resistance was accompanied by increased mitochondrial superoxide production, alterations in bioenergetics, and elevated mitochondrial content. These findings suggest that PFAS exposure induces chemotherapy resistance in ovarian cancer cells in a duration-dependent manner, worsened by human-relevant chronic exposures, and that mechanisms driving these effects are influenced by the modulation of mitochondrial parameters. Future studies should focus on targeting mechanisms underlying PFAS-induced chemotherapy resistance to improve survival outcomes.

Indexed as

Antineoplastic AgentsDrug Resistance, NeoplasmEnvironmental PollutantsFluorocarbonsMitochondriaOvarian NeoplasmsCarboplatinCell Line, TumorDoxorubicinFemaleHumansAntineoplastic AgentsCarboplatinDoxorubicinEnvironmental PollutantsFluorocarbonsChemoresistanceMitochondriaOvarian cancerPerfluoroalkyl substancesPFASPlatinum resistance

Identifiers

PMID40550304
PMCPMC12498143

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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.