Evidence map›Paper›PMID 41174639›Full record

ArticleJournal of ovarian research2025

ACSS2 promotes proliferation and invasiveness of SKOV-3 and PA-1 ovarian cancer cell lines under hypoxia.

Ola Mroweh, Louna Karam, Razane Hammoud, Jana Al Achcar, Rania Sobh, Selim M Nasser, Joseph A Garcia, Philippe Hussein Kobeissy

Abstract read
In one paragraph

Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Acetate Metabolism in Thyroid Cancer Progression.International journal of molecular sciences · 2026
    Article
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.

Ola Mroweh *School of Arts and Sciences, Department of Biological Sciences, Lebanese American University, Beirut, 1102-2801, Lebanon.
Louna Karam *School of Arts and Sciences, Department of Biological Sciences, Lebanese American University, Beirut, 1102-2801, Lebanon.
Razane HammoudSchool of Arts and Sciences, Department of Biological Sciences, Lebanese American University, Beirut, 1102-2801, Lebanon.
Jana Al AchcarSchool of Arts and Sciences, Department of Biological Sciences, Lebanese American University, Beirut, 1102-2801, Lebanon.
Rania SobhSchool of Medicine, Department of Pathology, Lebanese American University, P.O Box 36, Byblos, Lebanon.
Selim M NasserSchool of Medicine, Department of Pathology, Lebanese American University, P.O Box 36, Byblos, Lebanon.
Joseph A GarciaDepartment of Medicine, Columbia University Medical Center, New York, New York, United States of America.
Philippe Hussein KobeissySchool of Arts and Sciences, Department of Biological Sciences, Lebanese American University, Beirut, 1102-2801, Lebanon. Philippehussein.kobeissy@lau.edu.lb.

Funding

BLRD VA I01 BX000446BLRD VA I21 BX006263
6 · The paper itself

Abstract

objectiveOvarian cancer is the eighth most common malignancy among women worldwide. Despite advances in treatment, chemoresistance and associated morbidity remain significant challenges. This study aims to elucidate the role of acetate-dependent acetyl-CoA synthetase 2 (ACSS2) in ovarian cancer progression under hypoxic conditions, identifying its potential as a therapeutic target.

resultsImmunohistochemistry revealed that ACSS2 was overexpressed and predominantly localized to the nucleus in High-Grade Serous Ovarian Carcinoma (HGSOC) tissues, with significantly higher H-scores compared to low-grade and normal tissues. Functional assays conducted on ovarian cancer cell lines (Skov-3 and PA-1) demonstrated that ACSS2 inhibition reduced proliferation, colony formation, and three-dimensional spheroid growth, with greater sensitivity observed under hypoxic conditions. Migration and invasion assays further indicated that ACSS2 inhibition significantly impaired cellular motility and invasiveness, particularly in hypoxia. Mechanistic studies, including Western blotting and RT-qPCR, showed that ACSS2 inhibition modulated the PI3K pathway and downregulated Hypoxia-Inducible Factor 2 (HIF-2) levels as well as HIF-2-responsive genes expression under hypoxic conditions. These findings highlight the role of ACSS2 in metabolic adaptation, tumor progression, and its potential as a biomarker and therapeutic target in ovarian cancer.

conclusionsACSS2 is a critical regulator of ovarian cancer growth and invasiveness under hypoxic stress. Targeting ACSS2 may represent a promising therapeutic strategy for managing ovarian cancer. Further studies are warranted to explore its clinical potential.

Indexed as

Acetate-CoA LigaseOvarian NeoplasmsCell HypoxiaCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessAcetate-CoA LigaseACSS2 protein, humanACSS2HGSOCHIFHypoxiaOvarian cancerPI3KTumor microenvironment

Identifiers

PMID41174639
PMCPMC12577375

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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.