Prognostic value of the FUT family in acute myeloid leukemia

Dai, Yifeng; Cheng, Zhiheng; Pang, Yifan; Jiao, Yang; Qian, Tingting; Qin, Liang; Cui, Longzhen; Liu, Yan; Si, Chaozeng; Chen, Jinghong; Yang, Xu; Chen, Jingqi; Shi, Jianxin; Wu, Depei; Zhang, Xinyou; Fu, Lin

doi:10.1038/s41417-019-0115-9

Cited by 22 publications

(18 citation statements)

References 40 publications

(43 reference statements)

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“…33 FUT7 is a member of the fucosyltransferase family that is known to play a regulatory role in multivariate physiological and pathological processes, such as the formation of endometrial receptivity, 34 embryo implantation, 35 as well as cancer development and metastasis. 36 The overexpression of FUT7 was found in follicular thyroid carcinoma, 25 acute myeloid leukemia, 37 and hepatocarcinoma, 22 etc. To determine the role of FUT7 in BLCA, we first evaluated its expression profile and prognostic value by using Oncomine and PrognoScan databases.…”

Section: Discussionmentioning

confidence: 99%

FUT7 Promotes the Epithelial–Mesenchymal Transition and Immune Infiltration in Bladder Urothelial Carcinoma

Liu¹,

Zheng²,

Chen³

et al. 2021

JIR

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Background Bladder urothelial carcinoma (BLCA) is one of the most frequently appearing, lethal and aggressive malignancies of the genitourinary system with growing morbidity and mortality, which affects human health seriously. Protein glycosylation, catalyzed by specific glycosyltransferase, has been found to be abnormal in several diseases, especially cancer. Fucosyltransferase VII (FUT7), one of the fucosyltransferases, was observed abnormally expressed in various cancers, however, the role of FUT7 in BLCA, and the association between its expression and clinical outcomes or immune infiltration remains unclear. Methodology FUT7 expression in BLCA was analyzed in Oncomine database, which was further confirmed with immunohistochemistry and ELISA. The prognostic value of FUT7 for BLCA was evaluated with PrognoScan database, and its genetic alteration was examined in cBioPortal database. The proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) changes of bladder cancer cells after FUT7 siRNA or cDNA transfection were determined by CCK8, colony formation, transwell and Western blot, respectively. The correlation between FUT7 expression and immune infiltration levels was analyzed in TIMER and TISIDB databases, and the methylation level of FUT7 was detected in UALCAN database. Results The results showed that the expression of FUT7 was increased in BLCA, and patients with high FUT7 level were predicted to have lower overall survival and disease-specific survival rates, which were not influenced by FUT7 genetic alterations. Downregulation FUT7 inhibited the proliferation, migration, invasion and EMT of bladder cancer cells, whereas upregulation of FUT7 showed the opposite effects. We found that FUT7 was positively correlated with immune cell infiltration levels (CD8+ T cells, CD4+T cells, macrophage, neutrophil and dendritic cells), and also the expression of gene markers of immune cells. The negative correlation between FUT7 expression and FUT7 methylation level was observed, among which FUT7 expression was positively correlated with the abundance of 28 kinds of tumor-infiltrating lymphocytes (TILs), while FUT7 methylation level was negatively correlated with TILs. Conclusion Altogether, these findings suggested that FUT7 possessed the potential to serve as a detection biomarker or immunotherapeutic target for BLCA.

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Section: Discussionmentioning

confidence: 99%

FUT7 Promotes the Epithelial–Mesenchymal Transition and Immune Infiltration in Bladder Urothelial Carcinoma

Liu¹,

Zheng²,

Chen³

et al. 2021

JIR

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“…Some gene abnormalities have been identified as independent prognostic factors. For example, high expressions of FUT3/6/7, PDK2/3, PAK3/7 and NCALD were proved as poor prognosis factors in AML [4][5][6][7]. While high FUT4 and PAK2 expressers have longer EFS and OS after chemotherapy [4,6].…”

Section: Introductionmentioning

confidence: 99%

Prognostic significance of Spinster homolog gene family in acute myeloid leukemia

Huang¹,

Qian²,

Cheng³

et al. 2020

J. Cancer

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Acute myeloid leukemia (AML) is a clonal and heterogeneous disease characterized by proliferation of immature myeloid cells, with impaired differentiation and maturation. Spinster homolog (SPNS) is a widely distributed transmembrane transporter, which assists sphingolipids in playing their roles through the cell membrane. However, the expression and clinical implication of the SPNS family has not been investigated in AML. From the Cancer Genome Atlas database, a total of 155 AML patients with complete clinical characteristics and SPNS1-3 expression data were contained in our study. In patients who received chemotherapy only, high expressions of SPNS2 and SPNS3 had adverse effects on event-free survival (EFS) and overall survival (OS) (all P＜0.05). However, in the allogeneic hematopoietic stem cell transplantation (allo-HSCT) group, we only found a significant difference in OS between the high and low SPNS3 expression groups (P=0.001), while other SPNS members showed no effect on survival. Multivariate analysis indicated that high SPNS2 expression was an independent risk factor for both EFS and OS in chemotherapy patients. The results confirmed that high expression of SPNS2 and SPNS3 were poor prognostic factors, and the effect of SPNS2 can be neutralized by allo-HSCT.

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“…Aberrant glycosylation affects well-known intrinsic traits of tumors, such as proliferation, metastasis, angiogenesis, and drug resistance, among others [ 6 – 9 ]. Fucosylation is a significant kind of glycosylation that is catalyzed by fucosyltransferases (FUTs) [ 10 ]. FUTs can be divided into four types according to their catalytic products: FUT1-2, FUT3-7, FUT9-11, and FUT8 [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Alpha-(1,6)-fucosyltransferase (FUT8) affects the survival strategy of osteosarcoma by remodeling TNF/NF-κB2 signaling

et al. 2021

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Glycosylation is an important modification of membrane proteins that results in functional changes in many cellular activities, from cell-cell recognition to regulatory signaling. Fucosyltransferase 8 (FUT8) is the sole enzyme responsible for core fucosylation, and aberrant fucosylation by dysregulated expression of fucosyltransferases is responsible for the growth of various types of carcinomas. However, the function of FUT8 in the progress of osteosarcoma (OS) has not been reported. In this study, we found that FUT8 is expressed at lower levels in patients with OS and in human OS cell lines such as MNNG/HOS, U2OS, and 143B, suggesting that attenuated expression of FUT8 is involved in the growth and progression of OS. Mechanistically, FUT8 affects the survival strategy of OS by modifying core-fucosylation levels of TNF receptors (TNFRs). Lower fucosylation of TNFRs activates the non-canonical NF-κB signaling pathway, and in turn, decreases mitochondria-dependent apoptosis in OS cells. Together, our results point to FUT8 being a negative regulator of OS that enhances OS-cell apoptosis and suggests a novel therapeutic strategy for treating OS.

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Prognostic value of the FUT family in acute myeloid leukemia

Cited by 22 publications

References 40 publications

FUT7 Promotes the Epithelial–Mesenchymal Transition and Immune Infiltration in Bladder Urothelial Carcinoma

FUT7 Promotes the Epithelial–Mesenchymal Transition and Immune Infiltration in Bladder Urothelial Carcinoma

Prognostic significance of Spinster homolog gene family in acute myeloid leukemia

Alpha-(1,6)-fucosyltransferase (FUT8) affects the survival strategy of osteosarcoma by remodeling TNF/NF-κB2 signaling

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