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Backgrounds: Ovarian cancer (OC) is the second most common gynecological tumor with the highest mortality rate worldwide. High FAM111B expression has been reported as a predictor of poor prognosis in other cancers, but its correlation with OC has not been reported.
Methods: Immunohistochemistry of tissue microarrays was performed to detect FAM111B expression levels in 141 OC patient tissues. The prognostic value of FAM111B was determined by Kaplan-Meier survival analysis, and correlations between FAM111B expression and clinicopathologic features were investigated by the Clu-square test. The significance of FAM111B expression was verified bioinformatically using the Gene Expression Omnibus database. Protein-protein interaction were performed to explore downstream mechanisms of FAM111B in OC.
Results: Among 141 OC patients, FAM111B was positively expressed in 87.23%, 58.16%, and 87.94%; and highly expressed in 8.51%, 17.02%, and 19.86%, as evaluated by cytoplasmic, nuclear, and combined cytoplasmic/nuclear staining. FAM111B expression was positively correlated with the expression of tumor protein markers KI67, EGFR, and PDL-1. Patients with high FAM111B expression had aggressive clinicopathologic features and shorter overall survival (P value 0.0428, 0.0050, 0.0029) and progression-free survival (P value 0.0251, 0.012, 0.0596) compared to the low FAM111B expression group for cytoplasmic, nuclear, and combined cytoplasmic/nuclear groups, respectively. These results were verified using patient data from the Gene Expression Omnibus. Seventeen genes co-expressed with FAM111B were primarily involved in "negative regulation of histone modification", "hippo signaling" and "inner ear receptor cell differentiation".
Conclusions: High FAM111B expression may serve as a novel prognostic predictor and molecular therapeutic target for OC.
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http://dx.doi.org/10.1016/j.tranon.2023.101659 | DOI Listing |
EBioMedicine
August 2025
Nantes Université, CNRS, INSERM, l'institut du Thorax, Nantes 44000, France; Nantes Université, CHU Nantes, Service de Génétique Médicale, Nantes 44000, France. Electronic address:
Background: Poikiloderma, hereditary fibrosing, with tendon contractures, myopathy, and pulmonary fibrosis (POIKTMP) is a rare genetic multisystemic fibrosing disorder caused by FAM111B gene mutations. Given its rarity, the molecular underpinnings of POIKTMP remain elusive. FAM111B, a trypsin-like serine protease, initially studied in cancer, exhibits germline variants not consistently linked to tumours, suggesting broader functions beyond cell proliferation.
View Article and Find Full Text PDFCell Death Dis
August 2025
Department of General Surgery, Qilu Hospital of Shandong University, Jinan, China.
Lenvatinib resistance significantly limits its clinical efficacy and application in the treatment of hepatocellular carcinoma (HCC). Mitofusin 2 (MFN2) is an important GTPase involved in mitochondrial fusion, energy balance and mitophagy. The role and regulatory mechanism of MFN2 in HCC progression and lenvatinib resistance remain unclear.
View Article and Find Full Text PDFNeurol Res
August 2025
Department of Surgery of Spine and Spinal Cord, Henan Provincial People's Hospital; People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan, China.
Background: In recent years, FAM111B has been found to be closely related to the occurrence and development of various cancers. However, the role of FAM111B in low-grade glioma (LGG) remains unclear.
Objective: This study aims to investigate the regulatory role of FAM111B in the progression of LGG.
BMC Cancer
August 2025
Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background: Ovarian cancer, a prevalent malignancy with the highest fatality rate among gynecological cancers, continues to face challenges in the development of effectively targeted therapeutic approaches. While the FAM111B gene has been implicated in various cancer types, its specific role in ovarian cancer remains poorly understood.
Methods: The ES2 and A2780 ovarian cell lines were exploited to explore the cellular proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in FAM111B knockdown experiments.
Front Genet
June 2025
Department of Radiotherapy, Air Force Medical Center, Air Force Medical University, Beijing, China.
Purpose: Metabolic reprogramming plays a crucial role in multiple malignant features of pancreatic cancer (PC). However, few studies have comprehensively examined metabolic features of PC and provided guidance for their treatment.
Methods: This study tried to identify metabolism-associated hub genes based on metabolic phenotypic levels through weighted gene co-expression network analysis, and constructed a risk model for PC, then verified its accuracy and explored the potential mechanisms.