ArticleJournal of clinical laboratory analysis2022
Clinicopathological features, prognostic significance, and associated tumor cell functions of family with sequence similarity 111 member B in pancreatic adenocarcinoma.
Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Pan-cancer analysis identifies FAM111B as a biomarker for immune suppression microenvironment in low-grade gliomas.Translational cancer research · 2026Article
- FAM111B Suppression Enhances Sensitivity to Gemcitabine in Pancreatic Cancer Through Intracellular pH Regulation.Cancer science · 2025Article
- Exploration of signature-related FAM genes and correlation between FAM50A expression and the pathogenesis and prognosis of hepatocellular carcinoma.Translational cancer research · 2025Article
- The complex role and molecular mechanism of family with sequence similarity genes in cancer: a comprehensive review.Discover oncology · 2025Review
- FAM111B and FANCD2, a dual expression signature, defines a distinct phenotype of pancreatic cancer.Cancer cell international · 2025Article
- Unveiling FAM111B: A Pan-Cancer Biomarker for DNA Repair and Immune Infiltration.International journal of molecular sciences · 2025Article
- Metabolic reprogramming and prognostic modeling in pancreatic cancer: insights from WGCNA.Frontiers in genetics · 2025Article
- PRIM2 promotes proliferation and metastasis of pancreatic ductal adenocarcinoma through interactions with FAM111B.Medical oncology (Northwood, London, England) · 2024Article
- CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway.Archives of medical science : AMS · 2024Article
- Article
- Clinicopathological features, prognostic significance, and associated tumor cell functions of family with sequence similarity 111 member B in pancreatic adenocarcinoma.Journal of clinical laboratory analysis · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroudAmong digestive tract tumors, pancreatic adenocarcinoma (PAAD) has a high degree of malignancy. Therefore, it is important to search for pancreatic adenocarcinoma-related differential genes and new oncogene therapeutic targets for early diagnosis, treatment, and prognosis of pancreatic adenocarcinoma.
aimsThis study aims to investigate the expression and clinical significance of Family with sequence similarity 111 member B (FAM111B) in PAAD. MATERIALS &
methodsBioinformatics was used to analyze the relationship between FAM111B expression and pancreatic adenocarcinoma and to predict its role in related pathways. Tissue microarrays were used to assess the levels of FAM111B in pancreatic cancer tissues by immunohistochemical staining, and the effects of FAM111B expression levels on apoptosis, proliferation, invasion and migration of tumor cells were observed and verified by in vitro cellular assays.
resultsFAM111B expression was higher in PAAD tissue than in matched normal tissues (p < 0.05). The expression level of FAM111B, the metastatic status of lymph nodes was an independent prognostic factor for PAAD survival (p < 0.05). Meanwhile, overexpression of FAM111B promoted PAAD cell proliferation, migration, invasion and inhibited PAAD cell apoptosis (p < 0.05). In contrast, knockdown of FAM111B triggered the opposite result (p < 0.05). In the results of GSEA, it was shown that FAM111B may be involved in PAAD progression through p53 signaling pathway, cell cycle, and other signaling pathways (p < 0.05 and FDR q-val <0.25). FAM111B is highly expressed in PAAD tissues and is closely associated with poor prognosis of PAAD.
conclusionFAM111B significantly promotes the proliferation, invasion, and migration of pancreatic adenocarcinoma cells while it inhibits their apoptosis. FAM111B may be a new biomarker for PAAD. It may provide a new direction for the treatment and diagnosis of PAAD.
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