Ask about this productRelated genes to: FBXL16 antibody
- Gene:
- FBXL16 NIH gene
- Name:
- F-box and leucine rich repeat protein 16
- Previous symbol:
- C16orf22
- Synonyms:
- MGC33974, Fbl16
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-21
- Date modifiied:
- 2016-06-06
Related products to: FBXL16 antibody
Related articles to: FBXL16 antibody
- Idiopathic pulmonary fibrosis (IPF) is associated with poor prognosis. - Source: PubMed
Publication date: 2026/01/06
Yang WangPan Peng - Temozolomide (TMZ) resistance is a major cause of treatment failure in glioblastoma (GBM). This study investigates the role and mechanism of the RNA-binding protein RNA-binding motif protein 7 (RBM7) and F-box and leucine-rich repeat protein 16 (FBXL16) in TMZ resistance in GBM, focusing on mitochondrial dysfunction and ferroptosis. TMZ-resistant GBM cell lines (TR/U87) were established through gradient induction. Cell viability and proliferation were assessed using the Cell Counting Kit-8 assay and colony formation assays. Western blot analysis and immunohistochemistry were performed to measure FBXL16, activating transcription factor 4, and peroxisome proliferator-activated receptor gamma coactivator 1-alpha protein expression. Transwell assays evaluated TR/U87 cell migration and invasion. Co-immunoprecipitation and RNA immunoprecipitation assays verified the interaction between RBM7 and FBXL16. An actinomycin D assay analyzed FBXL16 mRNA stability. Flow cytometry was used to detect reactive oxygen species, iron levels, and apoptosis. A nude mouse xenograft model was used to validate in vivo effects. RBM7 was highly expressed in TMZ-resistant cells. Knockdown of RBM7 suppressed TR/U87 cell proliferation and migration, induced mitochondrial structural damage, and triggered ferroptosis. Mechanistically, RBM7 interacted with FBXL16 and reduced its mRNA stability. FBXL16 knockdown reversed RBM7 deficiency-induced ferroptosis and chemosensitivity. In vivo experiments confirmed that RBM7 knockdown combined with TMZ significantly inhibited tumor growth. RBM7 promotes TMZ resistance by suppressing mitochondrial dysfunction and ferroptosis through destabilization of FBXL16. Targeting the RBM7-FBXL16 axis may represent a novel strategy to overcome GBM chemoresistance. - Source: PubMed
Publication date: 2025/12/12
Liu NanCui YeTingLi JuanLi SuMeiTu YanYangHuo JunLiZhang TongCunZhen HaiNing - Gliomas are characterized by an immunosuppressive tumor microenvironment (TME), which significantly limits the efficacy of current immunotherapies. To address this challenge, we explored the role of FBXL16, a gene with distinct expression patterns in nervous system tumors identified through analysis of public databases. Our study utilized clinical sample analysis, survival correlation, in vitro functional assays, and in vivo mouse models to investigate FBXL16's impact on glioma progression. Gene set enrichment analysis (GSEA), immunosuppression profiling, and co-culture assays with flow cytometry validation were employed to elucidate its immunological role, particularly in regulating M2-type tumor-associated macrophage (M2-TAM) recruitment. Our investigation revealed a substantial decrease in FBXL16 expression within glioma tissues, which exhibited and positively correlation with patient survival rates. Overexpression of FBXL16 in glioma cells suppressed proliferation, migration, and invasion, and extended survival in glioma-bearing mice. Mechanistically, FBXL16 regulated the secretion of key immunoregulatory cytokines such as TGF-β, IL-6, IFN-α, and VEGF, thereby disrupting macrophage recruitment to the TME. These findings suggest that FBXL16 attenuates glioma progression by inhibiting cytokine release and limiting TAM recruitment, thus interrupting the immunosuppressive feedback loop within the TME. Our study highlights FBXL16 as a promising immunomodulatory target for glioma therapy, offering new insights into overcoming immunosuppression in gliomas. - Source: PubMed
Publication date: 2025/11/14
Fang ZhanshengLi JingyingXiong YuLuo PengxiangLu QiWu MiaojingHuang KaiZhang LongboZhu XingenWu Lei - Gliomas are a prevalent form of primary malignant brain tumor, yet the intricate molecular mechanisms underlying its pathogenesis remain unclear. This study aimed to identify new genetic targets linked to glioma by analyzing microarray datasets to uncover genetic factors involved in its onset and progression. We obtained two independent glioma datasets from the Gene Expression Omnibus database, processed and normalized them using R software, and evaluated the relationship between differentially expressed genes and glioma by differential expression, expression quantitative trait loci, and Mendelian randomization (MR) analyses. Gene set enrichment analysis and immunocytometric analysis further explored the biological functions and pathways of identified genes, which were validated using The Cancer Genome Atlas and Genotype-Tissue Expression datasets. We identified eight co-expressed genes-C1QB, GPX3, LRRC8B, TRIOBP, SNAPC5, SPI1, TSPYL5, and FBXL16-that are crucial in various biological processes. CIBERSORT analysis revealed significant immune cell-type distributions within gliomas, underscoring the significance of immune cell infiltration. Validation in additional datasets confirmed the MR analysis results and upstream regulatory factors were identified using NetworkAnalyst. Our findings offer fresh perspectives on the molecular underpinnings of glioma and highlight potential targets for therapeutic interventions. - Source: PubMed
Publication date: 2025/01/20
Pei ShiwenJiang ZhiquanCheng Hongwei - Endometrial carcinoma (EC) often exhibits resistance to hormone therapies, such as medroxyprogesterone acetate (MPA), highlighting the need for novel strategies to enhance therapeutic efficacy. The present study aimed to investigate the effects of polyphyllin VII (PPVII) on the efficacy of MPA in EC, focusing on the regulatory role of microRNA (miR)-33a-5p. Briefly, an MPA-resistant Ishikawa cell line (Ishikawa/MPA-R), maintained with 10 µM MPA, was established and transfected with negative control (NC) and miR-33a-5p inhibitors. Following treatment with PPVII and MPA, the proliferation capacity and apoptosis levels of the Ishikawa and Ishikawa/MPA-R cells were evaluated using reverse transcription-quantitative polymerase chain reaction, MTT assay, clonogenic assay, flow cytometry, western blotting and dual-luciferase assay. Next, the expression levels of miR-33a-5p and F-box and leucine rich repeat protein 16 (FBXL16) were measured, and the regulatory relationship between miR-33a-5p and FBXL16 was analyzed. Significant reductions in cell viability were observed in all groups following treatment with increased concentrations of MPA and PPVII, with the greatest effect observed in the combined MPA + PPVII group (P<0.01). The apoptosis levels of the Ishikawa/MPA-R cells were significantly increased in all drug treatment groups, particularly in the MPA + PPVII group (P<0.05). PPVII treatment significantly increased the expression level of miR-33a-5p in Ishikawa/MPA-R cells (P<0.01). In the PPVII + miR-33a-5p inhibitor group, the Ishikawa/MPA-R cells exhibited an upregulation in the viability (P<0.01), colony formation ability (P<0.01), proportion in the G1 phase (P<0.05) and the protein expression levels of cyclin D1 (P<0.01) and cyclin-dependent kinase 4 (P<0.01), and a reduction in the miR-33a-5p expression (P<0.01), apoptosis levels (P<0.05), proportion in the S (P<0.05) and G2 phases and the levels of Bcl-2-associated X protein (P<0.001). The FBXL16 protein expression in Ishikawa/MPA-R cells was significantly higher compared with Ishikawa cells, and the mRNA and protein expression levels of FBXL16 were markedly elevated in the PPVII + miR-33a-5p inhibitor group compared with the PPVII + NC group (P<0.01). These findings suggested that PPVII upregulated the expression of miR-33a-5p, enhanced the sensitivity of EC cells to MPA and potentially exerted anticancer effects in EC through the synergistic action of the miR-33a-5p/FBXL16 axis in combination with MPA. - Source: PubMed
Publication date: 2024/11/22
Liu HaoenPeng YanZhuang Xiaodan