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Cells
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Genomics and Cellular Mechanisms in Ovarian Cancer
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Genomics and Cellular Mechanisms in Ovarian Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 15 June 2026 | Viewed by 2862

Special Issue Editor

Dr. Hao Huang

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Northwestern University, Chicago, IL 60611, USA
Interests: ovarian cancer; epigenetics; immunology; signal transduction; drug resistance; targeted therapies

Special Issue Information

Dear Colleagues,

Ovarian cancer is one of the most lethal gynecologic malignancies, primarily due to its asymptomatic nature, late-stage diagnosis, and high rate of resistance to standard treatments such as platinum-based chemotherapy and PARP inhibitors. Despite advances in clinical management, long-term survival remains limited for many patients. However, the rapid development of high-throughput sequencing, single-cell technologies, and spatial transcriptomics has dramatically advanced our understanding of the molecular and cellular complexity of ovarian tumors. These technologies have uncovered critical oncogenic alterations—including mutations in TP53, BRCA1/2, and epigenetic regulators—as well as transcriptional programs associated with stemness, immune evasion, and metastasis. Moreover, growing evidence highlights the tumor microenvironment, including stromal and immune components, as a key driver of progression and treatment response.

This Special Issue invites original research and comprehensive reviews focused on the genomic and cellular mechanisms underlying ovarian cancer pathogenesis, therapeutic resistance, and clinical heterogeneity. We especially welcome studies that integrate multi-omics data, apply innovative experimental models, or identify new molecular targets with translational relevance. Topics of interest include genomic and epigenomic profiling, RNA modifications, single-cell and spatial analyses, tumor–immune interactions, and the functional validation of therapeutic strategies. Collectively, these contributions aim at promoting precision oncology and improving outcomes for patients with ovarian cancer.

Dr. Hao Huang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ovarian cancer
  • tumor heterogeneity
  • genomics and epigenomics
  • therapy resistance
  • tumor microenvironment

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Published Papers (3 papers)

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Research

22 pages, 5775 KB  
Article
Epitranscriptomic Regulation of Platinum Resistance via the METTL3-ADAM23 Axis in Ovarian Cancer
by Ujin Kim, Junzui Li, Daniela Matei and Hao Huang
Cells 2026, 15(3), 294; https://doi.org/10.3390/cells15030294 - 4 Feb 2026
Viewed by 832
Abstract
N6-methyladenosine (m6A) has emerged as a pivotal regulator of post-transcriptional gene control, yet its contribution to chemotherapy resistance remains insufficiently defined. Here, we describe a previously unrecognized METTL3-ADAM23 epitranscriptomic regulatory relationship associated with platinum (Pt) resistance in ovarian cancer (OC). We [...] Read more.
N6-methyladenosine (m6A) has emerged as a pivotal regulator of post-transcriptional gene control, yet its contribution to chemotherapy resistance remains insufficiently defined. Here, we describe a previously unrecognized METTL3-ADAM23 epitranscriptomic regulatory relationship associated with platinum (Pt) resistance in ovarian cancer (OC). We show that cisplatin treatment increases global m6A levels and METTL3 expression, linking Pt exposure to activation of the m6A machinery. Functional perturbation studies demonstrate that METTL3 overexpression enhances cisplatin resistance, whereas METTL3 knockdown or pharmacologic inhibition with the selective METTL3 inhibitor STM2457 sensitizes OC cells to Pt treatment in vitro and improves Pt response in vivo. Transcriptomic profiling identifies ADAM23, a cell-adhesion-related tumor suppressor, as a METTL3-dependent, m6A-associated transcript, with altered mRNA expression observed across multiple experimental systems and several high-confidence predicted m6A sites within its transcript. Cisplatin-associated METTL3 upregulation correlates with reduced ADAM23 expression, suggesting a potential regulatory relationship that may contribute to chemoresistance. Together, these findings support a model in which METTL3-associated increases in m6A methylation are linked to Pt resistance, in part through modulation of ADAM23 expression, and highlight METTL3 as a potential therapeutic target in OC. Full article
(This article belongs to the Special Issue Genomics and Cellular Mechanisms in Ovarian Cancer)
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22 pages, 11282 KB  
Article
Effects of N-Acetylcysteine and Alpha-Ketoglutarate on OVCAR3 Ovarian Cancer Cells: Insights from Integrative Bioinformatics and Experimental Validation
by Yasaman Khamineh, Sanaz Panahi-Alanagh, Samaneh Zolghadri, Laleh Mavaddatiyan, Ireneusz Ryszkiel, Agata Stanek and Mahmood Talkhabi
Cells 2026, 15(3), 281; https://doi.org/10.3390/cells15030281 - 2 Feb 2026
Viewed by 888
Abstract
Ovarian cancer remains one of the leading causes of cancer-related mortality among women, underscoring the need for novel combination strategies that effectively inhibit tumor cell growth while limiting adverse effects. N-acetylcysteine (NAC) and alpha-ketoglutarate (AKG) are biologically active compounds with reported anticancer properties; [...] Read more.
Ovarian cancer remains one of the leading causes of cancer-related mortality among women, underscoring the need for novel combination strategies that effectively inhibit tumor cell growth while limiting adverse effects. N-acetylcysteine (NAC) and alpha-ketoglutarate (AKG) are biologically active compounds with reported anticancer properties; however, their combined effects in ovarian cancer are not well characterized. In this study, we applied an integrative approach combining network pharmacology analysis with in vitro experiments to investigate the effects of NAC and AKG on OVCAR3 ovarian cancer cells. Common molecular targets of NAC and AKG were identified by intersecting predicted compound targets with ovarian cancer-associated genes, followed by protein–protein interaction network construction and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. Experimental validation assessed the effects of NAC and AKG, alone and in combination, on cell viability, apoptosis, migration, and clonogenic capacity. Network analysis identified 70 shared target genes enriched in pathways related to apoptosis, cellular stress responses, and cell migration. In vitro experiments demonstrated that combined treatment with NAC (10 mM) and AKG (100 µM) significantly reduced cell viability, increased apoptotic cell death, and markedly suppressed cell migration and colony formation compared with single-agent treatments. Overall, these findings indicate that the combination of NAC and AKG exerts enhanced inhibitory effects on ovarian cancer cell growth and motility in vitro. Full article
(This article belongs to the Special Issue Genomics and Cellular Mechanisms in Ovarian Cancer)
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19 pages, 3327 KB  
Article
Ovulation-Derived Fibronectin Promotes Peritoneal Seeding of High-Grade Serous Carcinoma Precursor Cells via Integrin β1 Signaling
by Che-Fang Hsu, Liang-Yuan Wang, Vaishnavi Seenan, Pao-Chu Chen and Tang-Yuan Chu
Cells 2026, 15(1), 80; https://doi.org/10.3390/cells15010080 - 4 Jan 2026
Viewed by 722
Abstract
High-grade serous ovarian carcinoma (HGSC) is predominantly diagnosed at advanced stages with extensive peritoneal metastasis. A pivotal early event in HGSC development is the peritoneal seeding of tumor cells originating from the fallopian tube epithelial (FTE) precursor lesions. Ovulation releases follicular fluid (FF), [...] Read more.
High-grade serous ovarian carcinoma (HGSC) is predominantly diagnosed at advanced stages with extensive peritoneal metastasis. A pivotal early event in HGSC development is the peritoneal seeding of tumor cells originating from the fallopian tube epithelial (FTE) precursor lesions. Ovulation releases follicular fluid (FF), which is known to contain oncogenic factors that promote FTE cell transformation. However, the specific mechanisms and factors within FF that drive the early metastatic seeding of precancerous FTE cells remain poorly defined. We investigated the role of FF in the peritoneal dissemination of FTE-derived cells, and the abundance of fibronectin (FN) as a potential key mediator. Functional assays were performed using FN-depleted FF to assess its impact on migration, invasion, anchorage-independent growth, and peritoneal attachment. The role of the fibronectin receptor, integrin β1 (ITGB1), and the signaling pathways were evaluated via knockdown studies. In vivo xenograft models were used to quantify peritoneal seeding, and mechanistic studies elucidated the involved signaling pathways. We identified FN as a critical component of FF, present at high concentrations (~210 µg/mL), that potently drives FTE cell migration, invasion, and peritoneal seeding. Depletion of FN from FF abrogated the majority of these pro-metastatic activities in vitro and led to a dramatic 82% reduction in peritoneal tumor seeding in vivo. Knockdown of ITGB1 similarly impaired seeding. Mechanistically, FF-derived FN activates the ITGB1/FAK-SRC signaling pathway to promote tumor cell motility and colonization. Our study establishes FF-fibronectin as an important regulator of the early peritoneal seeding of HGSC precursor cells. These findings reveal a direct link between ovulation and HGSC development, suggesting that targeting the FN-ITGB1 signaling axis may offer a novel preventive strategy for high-risk individuals. Full article
(This article belongs to the Special Issue Genomics and Cellular Mechanisms in Ovarian Cancer)
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