FANCI is Associated with Poor Prognosis and Immune Infiltration in Liver Hepatocellular Carcinoma

Hou, Yibo; Li, Jianing; Yu, Albert Cheung Hoi; Deng, Kailai; Chen, Jiawei; Wang, Zixian; Huang, Laiqiang; Ma, Shaohua; Dai, Xiaoyong

doi:10.7150/ijms.83760

Cited by 4 publications

(2 citation statements)

References 45 publications

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“…The high FANCI expression level may boost up tumor growth in lung adenocarcinoma by inhibiting M1 macrophages (34, 35). Additionally, FANCI expression in liver hepatocellular carcinoma showed a positive relationship with tumor infiltration levels (36). These results indicated that FANCI may regulate the immune microenvironment of tumors.…”

Section: Discussionmentioning

confidence: 73%

FANCI serve as a prognostic biomarker correlated with immune infiltrates in skin cutaneous melanoma

Cai,

Duan,

et al. 2023

Front. Immunol.

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BackgroundAs a member of tumor, Skin cutaneous melanoma (SKCM) poses a serious threat to people’s health because of its strong malignancy. Unfortunately, effective treatment methods for SKCM remain lacking. FANCI plays a vital role in the occurrence and metastasis of various tumor types. However, its regulatory role in SKCM is unclear. The purpose of this study was to explore the association of FANCI with SKCM.MethodsThis study investigated the expression of FANCI in GSE46517, GSE15605, and GSE114445 from the Gene Expression Omnibus database and The Cancer Genome Atlas (TCGA)-SKCM datasets using the package “limma” or “DESeq2” in R environment and also investigated the prognostic significance of FANCI by utilizing the GEPIA database. Additionally, our research made use of real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemical (IHC) staining to verify FANCI expression between SKCM and normal tissues and developed the knockdown of FANCI in A375 and A875 cells to further analyze the function of FANCI. Finally, this study analyzed the correlation of FANCI and tumor-infiltrating immune cells by CIBERSORT, ESTIMATE, and ssGSEA algorithms.ResultsThe FANCI level was increasing in SKCM tissues from GSE46517, GSE15605, GSE114445, and TCGA-SKCM. However, high FANCI expression correlated with poor overall survival. The RT-qPCR and IHC confirmed the accuracy of bioinformatics. Knocking down FANCI suppresses A375 and A875 cell proliferation, migration, and invasion. FANCI could be involved in the immunological milieu of SKCM by regulating immune responses and infiltrating numerous immune cells, particularly neutrophils, CD8+ T cells, and B cells. Furthermore, patients with SKCM who have a high FANCI expression level are reported to exhibit immunosuppression, whereas those with a low FANCI expression level are more likely to experience positive outcomes from immunotherapy.ConclusionsThe increased FANCI expression in SKCM can be a prognostic biomarker. Knockdown FANCI can reduce the occurrence and progression of SKCM. The FANCI expression provides a foundation for predicting the immune status and treatment of SKCM.

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Section: Discussionmentioning

confidence: 73%

FANCI serve as a prognostic biomarker correlated with immune infiltrates in skin cutaneous melanoma

Cai,

Duan,

et al. 2023

Front. Immunol.

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“…The expression of NF-κB-p65 (RelA) and TNFα in GBM was utilized to create the overall survival (OS) curves; patients with a high level of expression (>median expression value) and patients with a low level of expression (<median expression value) were defined. The Kaplan-Meier (KM) method was used to evaluate overall survival using a log-rank test (statistically significant: p-value < 0.05) and to determine the hazards ratio (HR) with a 95% confidence interval [19]. In order to validate patient survival statistics, through UALCAN, we also ascertained the amounts of NF-κB p65 (RelA) and TNFα gene expression in GBM and also determined the functionality of genes that affected the patients' survival times.…”

Section: Bioinformatics Analysismentioning

confidence: 99%

Celecoxib Suppresses NF-κB p65 (RelA) and TNFα Expression Signaling in Glioblastoma

Ahsan,

Malik,

Shah

et al. 2023

JCM

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Background: Glioblastoma (GBM) harbors significant genetic heterogeneity, high infiltrative capacity, and patterns of relapse following many therapies. The expression of nuclear factor kappa-B (NF-κB p65 (RelA)) and signaling pathways is constitutively activated in GBM through inflammatory stimulation such as tumor necrosis factor-alpha (TNFα), cell invasion, motility, abnormal physiological stimuli, and inducible chemoresistance. However, the underlying anti-tumor and anti-proliferative mechanisms of NF-κB p65 (RelA) and TNFα are still poorly defined. This study aimed to investigate the expression profiling of NF-κB p65 (RelA) and TNFα as well as the effectiveness of celecoxib along with temozolomide (TMZ) in reducing the growth of the human GBM cell line SF-767. Methods: genome-wide expression profiling, enrichment analysis, immune infiltration, quantitative expression, and the Microculture Tetrazolium Test (MTT) proliferation assay were performed to appraise the effects of celecoxib and TMZ. Results: demonstrated the upregulation of NF-κB p65 (RelA) and TNFα and celecoxib reduced the viability of the human glioblastoma cell line SF-767, cell proliferation, and NF-κB p65 (RelA) and TNFα expression in a dose-dependent manner. Overall, these findings demonstrate for the first time how celecoxib therapy could mitigate the invasive characteristics of the human GBM cell line SF-767 by inhibiting the NF-κB mediated stimulation of the inflammatory cascade. Conclusion: based on current findings, we propose that celecoxib as a drug candidate in combination with temozolomide might dampen the transcriptional and enzymatic activities associated with the aggressiveness of GBM and reduce the expression of GBM-associated NF-κB p65 (RelA) and TNFα inflammatory genes expression.

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A novel disulfide death-related genes prognostic signature identifies the role of IPO4 in glioma progression

Wu,

Yang,

Chang

et al. 2024

Cancer Cell Int

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Background “Disulfide death,” a form of cellular demise, is triggered by the abnormal accumulation of intracellular disulfides under conditions of glucose deprivation. However, its role in the prognosis of glioma remains undetermined. Therefore, the main objective of this study is to establish prognostic signature based on disulfide death-related genes (DDRGs) and to provide new solutions in choosing the effective treatment of glioma. Methods The RNA transcriptome, clinical information, and mutation data of glioma samples were sourced from The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA), while normal samples were obtained from the Genotype-Tissue Expression (GTEx). DDRGs were compiled from previous studies and selected through differential analysis and univariate Cox regression analysis. The molecular subtypes were determined through consensus clustering analysis. Further, LASSO analysis was employed to select characteristic genes, and subsequently, a risk model comprising seven DDRGs was constructed based on multivariable Cox analysis. Kaplan-Meier survival curves were employed to assess survival differences between high and low-risk groups. Additionally, functional analyses (GO, KEGG, GSEA) were conducted to explore the potential biological functions and signaling pathways of genes associated with the model. The study also explored immune checkpoint (ICP) genes, immune cell infiltration levels, and immune stromal scores. Finally, the effect of Importin-4(IPO4) on glioma has been further confirmed through RT-qPCR, Western blot, and cell functional experiments. Results 7 genes associated with disulfide death were obtained and two subgroups of patients with different prognosis and clinical characteristics were identified. Risk signature was subsequently developed and proved to serve as an prognostic predictor. Notably, the high-risk group exhibited an immunosuppressive microenvironment characterized by a high concentration of M2 macrophages and regulatory T cells (Tregs). In contrast, the low-risk group showed lower half-maximal inhibitory concentration (IC50) values. Therefore, patients in the high-risk group may benefit more from immunotherapy, while patients in the low-risk group may benefit more from chemotherapy. In addition, in vitro experiments have shown that inhibition of the expression of IPO4 leads to a significant reduction in the proliferation, migration, and invasion of glioma cells. Conclusion This study identified two glioma subtypes and constructed a prognostic signature based on DDRGs. The signature has the potential to optimize the selection of patients for immune- and chemotherapy and provided a potential therapeutic target for glioma.

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FANCI is Associated with Poor Prognosis and Immune Infiltration in Liver Hepatocellular Carcinoma

Cited by 4 publications

References 45 publications

FANCI serve as a prognostic biomarker correlated with immune infiltrates in skin cutaneous melanoma

FANCI serve as a prognostic biomarker correlated with immune infiltrates in skin cutaneous melanoma

Celecoxib Suppresses NF-κB p65 (RelA) and TNFα Expression Signaling in Glioblastoma

A novel disulfide death-related genes prognostic signature identifies the role of IPO4 in glioma progression

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