Elevated GALNT10 expression identifies immunosuppressive microenvironment and dismal prognosis of patients with high grade serous ovarian cancer

Zhang, Guodong; Lü, Jiaqi; Yang, Moran; Wang, Yiying; Liu, Haiou; Xu, Congjian

doi:10.1007/s00262-019-02454-1

Cited by 27 publications

(20 citation statements)

References 43 publications

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“…26,27 Abnormal glycosylation is a common phenomenon that has been observed in cancer, and it can determine cancer stage, grade, and the fate of cancer progression. [28][29][30] It is a contributor to the occurrence and development of cancers, including bladder cancer. Deb et al carried out LC-MS/MSbased quantitative proteomic and glycoproteomic profiling analysis of glycosite-containing peptides and found aberrant protein glycosylation would provide additional avenues to employ glycan-based therapies and may lead to the identification of novel therapeutic targets.…”

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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“…Glycosylation can remarkably affect tumor invasion and immune escape. Zhang found that the high expression of GALNT10 in high-grade ovarian serous cancer (HGSC) is related to immunosuppressive microenvironment, thus promoting tumor progression (Zhang et al, 2020). No reports focus on studying the effect of the remaining genes on cancer.…”

Section: Discussionmentioning

confidence: 99%

Development and Validation of a Novel Metabolic-Related Signature Predicting Overall Survival for Pancreatic Cancer

Huo

Zang

2021

Front. Genet.

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Recently, growing evidence has revealed the significant effect of reprogrammed metabolism on pancreatic cancer in relation to carcinogenesis, progression, and treatment. However, the prognostic value of metabolism-related genes in pancreatic cancer has not been fully revealed. We identified 379 differentially expressed metabolic-related genes (DEMRGs) by comparing 178 pancreatic cancer tissues with 171 normal pancreatic tissues in The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression project (GTEx) databases. Then, we used univariate Cox regression analysis together with Lasso regression for constructing a prognostic model consisting of 15 metabolic genes. The unified risk score formula and cutoff value were taken into account to divide patients into two groups: high risk and low risk, with the former exhibiting a worse prognosis compared with the latter. The external validation results of the International Cancer Genome Consortium (IGCC) cohort and the Gene Expression Omnibus (GEO) cohort further confirm the effectiveness of this prognostic model. As shown in the receiver operating characteristic (ROC) curve, the area under curve (AUC) values of the risk score for overall survival (OS), disease-specific survival (DSS), and progression-free survival (PFS) were 0.871, 0.885, and 0.886, respectively. Based on the Gene Set Enrichment Analysis (GSEA), the 15-gene signature can affect some important biological processes and pathways of pancreatic cancer. In addition, the prognostic model was significantly correlated with the tumor immune microenvironment (immune cell infiltration, and immune checkpoint expression, etc.) and clinicopathological features (pathological stage, lymph node, and metastasis, etc.). We also built a nomogram based on three independent prognostic predictors (including individual neoplasm status, lymph node metastasis, and risk score) for the prediction of 1-, 3-, and 5-year OS of pancreatic cancer, which may help to further improve the treatment strategy of pancreatic cancer.

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“…GALNT10, a member of the N-acetylgalactosaminyltransferases (GALNT) family, has been studied in a variety of cancers [29]. GALNT10 can be applied as an independent prognostic factor for advanced ovarian serous carcinoma, which can predict poor prognosis and promote tumor progression [30]. Moreover, GALNT10 is up-regulated via HBV mediated inhibition of miR-122 and functioned as an oncogene in the progression of hepatocellular carcinoma [31].…”

Section: Discussionmentioning

confidence: 99%

The long noncoding RNA DLGAP1‐AS2 facilitates cholangiocarcinoma progression via miR‐505 and GALNT10

et al. 2020

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Cholangiocarcinoma (CCA) is a highly invasive malignant tumor with high mortality. Most cases of CCA are already advanced when they are detected, resulting in poor prognosis. As such, there is an ongoing need for the identification of effective biomarkers for CCA. The long noncoding RNA DLGAP1-AS2 has been reported to have prognostic value in glioma and Wilms' tumor. Here, we investigated the function of DLGAP1-AS2 in CCA. The differential expression of DLGAP1-AS2 in CCA tissues and normal tissues was first examined using data from the The Cancer Genome Atlas database and then in CCA cell lines by quantitative RT-PCR (qRT-PCR). The target gene was predicted by bioinformatics analysis, and the binding sites were confirmed using luciferase assay. DLGAP1-AS2 is upregulated in CCA, and high DLGAP1-AS2 expression promotes cell viability and is associated with poor prognosis. Notably, DLGAP1-AS2 acts as a sponge to suppress miR-505 expression, and miR-505 reduces the expression of N-acetylgalactosaminyltransferase 10 (GALNT10) in CCA cells. Biofunctional experiments revealed that a miR-505 inhibitor almost completely removed the inhibitory effect of si-DLGAP1-AS2 on CCA cell malignant progression, whereas the malignant phenotype of cells cotransfected with si-DLGAP1-AS2 and si-GALNT10 was significantly reduced as compared with the control. In summary, the DLGAP1-AS2/miR-505/ GALNT10 axis may contribute to regulating the malignant progression of CCA and may have potential as a novel target for CCA therapy. Cholangiocarcinoma (CCA) is a highly invasive malignant tumor with high mortality, which originated from the epithelial cells of bile ducts [1]. In recent decades, despite the difference in incidence rate and etiology of CCA in the world, the incidence rate of CCA has been presented as an upward trend worldwide [2]. Until now, radical resection was the most valid treatment for CCA [3]. However, because of the insidious onset and rapid progress of CCA, most patients with CCA are in advanced stage when they are diagnosed clinically, thus losing the opportunity of radical operation, and have a poor prognosis [4,5]. Hence it is important to master the molecular mechanism of CCA development for the study of effective biomarkers and therapeutic strategies. Recent studies have found that long noncoding RNA (lncRNA) is a class of macromolecular noncoding RNA that mainly regulated gene expression in the

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Elevated GALNT10 expression identifies immunosuppressive microenvironment and dismal prognosis of patients with high grade serous ovarian cancer

Cited by 27 publications

References 43 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

Development and Validation of a Novel Metabolic-Related Signature Predicting Overall Survival for Pancreatic Cancer

The long noncoding RNA DLGAP1‐AS2 facilitates cholangiocarcinoma progression via miR‐505 and GALNT10

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