FUT8 (Fucosyltransferase 8)

Moreover, the expression of E2F4, a transcription factor upregulated upon TGF-β stimulation, was shown to directly regulate the expression of FUT8 via a TGF-β-induced non-Smad signalling pathway. Our results elucidated a new mechanism facilitated by E2F4-FUT8-mediated receptor core fucosylation that promotes TGF-β signalling and EMT, ultimately driving the invasion and metastasis of GBM cells.

WHPB targets CSF-1R to suppress FUT8 via PI3K/AKT signaling, blocking key fibrotic pathways. These findings support WHPB's development as a targeted therapy that suppresses FUT8 for RIF.

Our findings highlight the critical role of circFUT8 in lung cancer progression through its regulation of M2 macrophage polarization via interaction with ENO1. The findings suggest that circFUT8 may serve as both a diagnostic marker and a promising therapeutic target in lung cancer management. This study first identified the regulating oncogenic role of circFUT8 in lung cancer progression and the microenvironment.

FUT8 is a crucial gene that causes colon cancer and is linked to tumour immunity. VE-822 is a promising candidate for treating CRC by targeting FUT8.

Collectively, these findings highlight the METTL14/FMR1 signaling axis could enhance circFUT8 expression to inhibit BCa cells growth and migration. CircFUT8 thus represents a promising target for therapeutic intervention and provides novel mechanistic insights into the epigenetic regulation of BCa progression.

Our study cements FUT8-mediated core fucosylation as an important driver of prostate cancer progression and suggests targeting FUT8 activity for prostate cancer therapy as an exciting area to explore.

Immunologically, FUT8 expression was significantly associated with immune cell infiltration and immune checkpoint activity, with a notable positive correlation with M2 macrophage infiltration. Our analysis of FUT8 indicates that it may serve as a potential biomarker for lung cancer diagnosis and prognosis, and could represent a therapeutic target for LUAD and LUSC immunotherapy.

Our in vitro and in vivo experiments reveal that circFUT8 upregulates HNRNPC by sponging miR-185-5p, thus enhancing NSCLC cell proliferation, migration, and invasion while reducing apoptosis and sensitivity to cisplatin. These findings highlight the circFUT8/miR-185-5p/HNRNPC axis as a potential target to overcome chemoresistance in NSCLC.

Simultaneous detection of FUT8, STX4, and calpain2 expression in ovarian tumor tissues provides valuable diagnostic insights for malignant ovarian tumors.

Mechanistically, RACK1 increased the expression of FUT8 by inhibiting miR-1275, which in turn promoted the FUT8-catalyzed core-fucosylation of cystine/glutamate antiporter SLC7A11, thereby inhibiting SLC7A11 degradation and cell ferroptosis. Our data highlight the role of RACK1 in cervical cancer progression and its suppression of ferroptosis via the RACK1/miR-1275/FUT8/SLC7A11 axis, suggesting that inhibiting this pathway may be a promising therapeutic approach for patients with cervical cancer.

As an example, recombinant antibodies derived from Chinese hamster ovary (CHO) cells are generally highly fucosylated; the absence of α1,6-fucose significantly enhances antibody-dependent cell-mediated cytotoxicity (ADCC) against cancer cells. This chapter describes a protocol applying clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated protein 9 (Cas9) approach with different formats to disrupt the α-1,6-fucosyltransferase (FUT8) gene and subsequently inhibit α-1,6 fucosylation on antibodies expressed in CHO cells.

This data is available via ProteomeXchange with identifier PXD050012. Overall, the results obtained merit further investigation to validate their feasibility as biomarkers of progression and malignization in CRC, as well as their potential usefulness in clinical practice.