Molecular and Clinical Characterization of a Novel Prognostic and Immunologic Biomarker FAM111A in Diffuse Lower-Grade Glioma

Ji, Xiaoshuai; Ding, Feng; Gao, Jiajia; Huang, Xiaoming; Liu, Wenqing; Wang, Yunda; Liu, Qian; Xin, Tao

doi:10.3389/fonc.2020.573800

Cited by 12 publications

(8 citation statements)

References 43 publications

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“…Through protecting replication forks, FAM111A was revealed to promote cell survival after drug treatment 54 . FAM111A was also reported to be associated with poor prognosis of diffuse lower‐grade glioma, the risk of aggressive prostate cancer, and distal metastases of cervical cancer 55–57 . Here, we also found that FAM111A was increased in HCC and correlated with poor survival of HCC patients.…”

Section: Discussionsupporting

confidence: 59%

N⁶‐methyladenosine‐modified FAM111A‐DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A

Huang

et al. 2023

Cancer Science

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As an epitranscriptomic modulation manner, N6‐methyladenosine (m6A) modification plays important roles in various diseases, including hepatocellular carcinoma (HCC). m6A modification affects the fate of RNAs. The potential contributions of m6A to the functions of RNA still need further investigation. In this study, we identified long noncoding RNA FAM111A‐DT as an m6A‐modified RNA and confirmed three m6A sites on FAM111A‐DT. The m6A modification level of FAM111A‐DT was increased in HCC tissues and cell lines, and increased m6A level was correlated with poor survival of HCC patients. m6A modification increased the stability of FAM111A‐DT transcript, whose expression level showed similar clinical relevance to that of the m6A level of FAM111A‐DT. Functional assays found that only m6A‐modified FAM111A‐DT promoted HCC cellular proliferation, DNA replication, and HCC tumor growth. Mutation of m6A sites on FAM111A‐DT abolished the roles of FAM111A‐DT. Mechanistic investigations found that m6A‐modified FAM111A‐DT bound to FAM111A promoter and also interacted with m6A reader YTHDC1, which further bound and recruited histone demethylase KDM3B to FAM111A promoter, leading to the reduction of the repressive histone mark H3K9me2 and transcriptional activation of FAM111A. The expression of FAM111A was positively correlated with the m6A level of FAM111A‐DT, and the expression of methyltransferase complex, YTHDC1, and KDM3B in HCC tissues. Depletion of FAM111A largely attenuated the roles of m6A‐modified FAM111A‐DT in HCC. In summary, the m6A‐modified FAM111A‐DT/YTHDC1/KDM3B/FAM111A regulatory axis promoted HCC growth and represented a candidate therapeutic target for HCC.

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Section: Discussionsupporting

confidence: 59%

N⁶‐methyladenosine‐modified FAM111A‐DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A

Huang

et al. 2023

Cancer Science

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“…We have reported in a previous study that in LGG, FAM111A can be used as a new type of immune-related biomarker ( 5 ). When we reviewed the data, we found that the expression of the BTN/BTNL (butyrophilins/butyrophilin-like) family in LGG was highly associated with FAM111A, which attracted our attention.…”

Section: Discussionmentioning

confidence: 99%

“…In our previous study, it was found that FAM111A was involved in regulating immune function in low-grade glioma (LGG) ( 5 ). On this basis, we further found that members of the BTN (butyrophilin)/BTNL (butyrophilin-like) subfamilies were highly correlated with the expression status of FAM111A, which caught our attention.…”

Section: Introductionmentioning

confidence: 99%

Comprehensive Analysis of the Prognostic Value and Immune Infiltration of Butyrophilin Subfamily 2/3 (BTN2/3) Members in Pan-Glioma

Qin

Liu

et al. 2022

Front. Oncol.

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The BTN2/3 subfamilies are overexpressed in many cancers, including pan-glioma (low- and high-grade gliomas). However, the expression and prognosis of BTN2/3 subfamilies and tumor-infiltrating lymphocytes in pan-glioma remain unknown. In the present study, we systematically explored and validated the expression and prognostic value of BTN2/3 subfamily members in pan-glioma [The Cancer Genome Atlas–glioblastoma and low-grade glioma (TCGA-GBMLGG) merge cohort] using multiple public databases. We used clinical specimens for high-throughput verification and cell lines for qRT-PCR verification, which confirmed the expression profiles of BTN2/3 subfamilies. In addition, the function of the BTN2/3 subfamily members and the correlations between BTN2/3 subfamily expression and pan-glioma immune infiltration levels were investigated. We found that BTN2/3 subfamily members were rarely mutated. BTN2/3 subfamilies were overexpressed in pan-glioma; high expression of BTN2/3 subfamily members was correlated with poor prognosis. In addition, BTN2/3 subfamilies might positively regulate proliferation, and the overexpression of BTN2/3 subfamilies influenced cell cycle, differentiation, and glioma stemness. In terms of immune infiltrating levels, BTN2/3 subfamily expression was positively associated with CD4+ T-cell, B-cell, neutrophil, macrophage, and dendritic cell infiltrating levels. These findings suggest that BTN2/3 subfamily expression is correlated with prognosis and immune infiltration levels in glioma. Therefore, the BTN2/3 subfamilies can be used as biomarkers for pan-glioma and prognostic biomarkers for determining the prognosis and immune infiltration levels in pan-glioma.

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“…For example, macrophages M2-dominated immune landscape promoted the proliferation and invasion of glioma cells [14][15][16][17][18] . However, the mechanisms of macrophage recruitment in glioma, or interaction between glioma cells and macrophages, were still scattered [19][20][21][22] . After an extensive literature review, we found that ligand-receptor molecules called immune checkpoints usually functioned as an "immune switch" to prevent autoimmune diseases by stabilizing the immune system.…”

Section: Introductionmentioning

confidence: 99%

Immunological and Prognostic Role of Cell Differentiation Trajectory Defined Gene Signature in Glioma

Hua

Cheng

Dai

et al. 2023

Preprint

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Glioma was characterized by its severe cellular heterogeneity during cell differentiation. Based on scRNA-seq and high throughput sequencing data, this research revealed the potential connections between cell differentiation trajectory and immune landscape in glioma. Glioma differentiation-related genes (GDRGs) were extracted from cell differentiation trajectories to establish a three-subtype molecular classification. Enrichment analysis indicated that GDRGs were involved in cell differentiation, intercellular adhesion, cytotoxicity, and cell cycle. ESTIMATE and CIBERSORT analysis showed that GDRGs and macrophages-related immune checkpoints (CD163, CD206, LILRB4, LILRB2, LILRB1, CD47, and SIRPα) promoted M2-dominated immune landscape in glioma. Finally, a novel prognostic risk score (RS) signature and nomogram based on 8 GDRGs (SOX4, MEX3A, EGFR, NES, ENC1, NEFL, NNAT, and TMSB15A) were established to predict the patient's 3-years and 5-years OS In conclusion, the molecular subtypes defined by cell differentiation trajectories predicted the M2-dominated immune landscape. GDRGs named SOX4, MEX3A, EGFR, NES, ENC1, NEFL, NNAT, and TMSB15A could be regarded as novel prognostic signatures and potential targets for immunotherapy.

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Molecular and Clinical Characterization of a Novel Prognostic and Immunologic Biomarker FAM111A in Diffuse Lower-Grade Glioma

Cited by 12 publications

References 43 publications

N⁶‐methyladenosine‐modified FAM111A‐DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A

N⁶‐methyladenosine‐modified FAM111A‐DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A

Comprehensive Analysis of the Prognostic Value and Immune Infiltration of Butyrophilin Subfamily 2/3 (BTN2/3) Members in Pan-Glioma

Immunological and Prognostic Role of Cell Differentiation Trajectory Defined Gene Signature in Glioma

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Molecular and Clinical Characterization of a Novel Prognostic and Immunologic Biomarker FAM111A in Diffuse Lower-Grade Glioma

Cited by 12 publications

References 43 publications

N6‐methyladenosine‐modified FAM111A‐DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A

N6‐methyladenosine‐modified FAM111A‐DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A

Comprehensive Analysis of the Prognostic Value and Immune Infiltration of Butyrophilin Subfamily 2/3 (BTN2/3) Members in Pan-Glioma

Immunological and Prognostic Role of Cell Differentiation Trajectory Defined Gene Signature in Glioma

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N⁶‐methyladenosine‐modified FAM111A‐DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A

N⁶‐methyladenosine‐modified FAM111A‐DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A