Evidence map›Paper›PMID 39519311›Full record

ArticleInternational journal of molecular sciences2024

Role of Peroxisome Proliferator-Activated Receptor α-Dependent Mitochondrial Metabolism in Ovarian Cancer Stem Cells.

Seo Yul Lee, Min Joo Shin, Seong Min Choi, Dae Kyoung Kim, Mee Gyeon Choi, Jun Se Kim, Dong Soo Suh, Jae Ho Kim, Seong Jang Kim

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. 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

9 authors.

Seo Yul LeeDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Gyeongsangnam-do, Republic of Korea.ORCID 0000-0003-4415-0070
Min Joo ShinDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Gyeongsangnam-do, Republic of Korea.ORCID 0000-0002-7786-5980
Seong Min ChoiDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Gyeongsangnam-do, Republic of Korea.
Dae Kyoung KimHiCellTech Inc., Yangsan 50612, Gyeongsangnam-do, Republic of Korea.
Mee Gyeon ChoiDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Gyeongsangnam-do, Republic of Korea.
Jun Se KimDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Gyeongsangnam-do, Republic of Korea.
Dong Soo SuhDepartment of Obstetrics and Gynecology, School of Medicine, Pusan National University, Yangsan 50612, Gyeongsangnam-do, Republic of Korea.
Jae Ho KimDepartment of Physiology, School of Medicine, Pusan National University, Yangsan 50612, Gyeongsangnam-do, Republic of Korea.ORCID 0000-0003-4323-4790
Seong Jang KimDepartment of Nuclear Medicine, School of Medicine, Pusan National University, Yangsan 50612, Gyeongsangnam-do, Republic of Korea.

Funding

National Research Foundation of Korea NRF-2022R1A5A2027161National Research Foundation of Korea NRF-2023R1A2C1006159
6 · The paper itself

Abstract

Peroxisome proliferator-activated receptors (PPARs), including PPAR-α, PPAR-β/δ, and PPAR-γ, are involved in various cellular responses, including metabolism and cell proliferation. Increasing evidence suggests that PPARs are closely associated with tumorigenesis and metastasis. However, the exact role of PPARs in energy metabolism and cancer stem cell (CSC) proliferation remains unclear. This study investigated the role of PPARs in energy metabolism and tumorigenesis in ovarian CSCs. The expression of PPARs and fatty acid consumption as an energy source increased in spheroids derived from A2780 ovarian cancer cells (A2780-SP) compared with their parental cells. GW6471, a PPARα inhibitor, induced apoptosis in A2780-SP. PPARα silencing mediated by small hairpin RNA reduced A2780-SP cell proliferation. Treatment with GW6471 significantly inhibited the respiratory oxygen consumption of A2780-SP cells, with reduced dependency on fatty acids, glucose, and glutamine. In a xenograft tumor transplantation mouse model, intraperitoneal injection of GW6471 inhibited in vivo tumor growth of A2780-SP cells. These results suggest that PPARα plays a vital role in regulating the proliferation and energy metabolism of CSCs by altering mitochondrial activity and that it offers a promising therapeutic target to eradicate CSCs.

Indexed as

Cell ProliferationMitochondriaNeoplastic Stem CellsOvarian NeoplasmsPPAR alphaAnimalsApoptosisCell Line, TumorEnergy MetabolismFatty AcidsFemaleHumansMiceMice, NudeOxazolesTyrosineFatty AcidsGW 6471OxazolesPPAR alphaTyrosinecancer stem cellsmetabolismmitochondriaovarian cancerPPARα

Identifiers

PMID39519311
PMCPMC11546303

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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.