ArticleAmerican journal of cancer research2019
DSE regulates the malignant characters of hepatocellular carcinoma cells by modulating CCL5/CCR1 axis.
Article in American journal of cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Identification and validation of a metabolism-related gene signature for predicting the prognosis of paediatric medulloblastoma.Scientific reports · 2024Article
- DSE inhibits melanoma progression by regulating tumor immune cell infiltration and VCAN.Cell death discovery · 2023Article
- Reconstruction of the regulatory hypermethylation network controlling hepatocellular carcinoma development during hepatitis C viral infection.Journal of integrative bioinformatics · 2023Article
- SNAP25 is a potential prognostic biomarker for prostate cancer.Cancer cell international · 2022Article
- Article
- Targeting Chemokine Receptor CCR1 as a Potential Therapeutic Approach for Multiple Myeloma.Frontiers in endocrinology · 2022Review
- Article
- Article
- Role of chemokines in hepatocellular carcinoma (Review).Oncology reports · 2021Review
- CHPF promotes malignancy of breast cancer cells by modifying syndecan-4 and the tumor microenvironment.American journal of cancer research · 2021Article
- Transcriptome sequencing analysis of mono‑ADP‑ribosylation in colorectal cancer cells.Oncology reports · 2020Article
- Broad and thematic remodeling of the surfaceome and glycoproteome on isogenic cells transformed with driving proliferative oncogenes.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal expression of dermatan sulfate epimerase (DSE) has been found in many types of cancer, while its expression and biological functions in hepatocellular carcinoma (HCC) progression remains obscure. Here we report that DSE, the enzyme that catalyzes the conversion of chondroitin sulfate (CS) to dermatan sulfate (DS), is a critical mediator of malignant character in HCC, through regulation of CCL5 signaling. DSE mRNA and protein were downregulated frequently in HCC tumors, where these events were associated with advanced tumor stages, metastases, and poor survival. DSE-mediated tumor growth was evaluated in immune-deficient and immune-complement mice models. Restoring DSE expression in HCC cells suppressed tumor growth, as well as decreased IL-1β and CCL5 levels in transplanted tumor tissue. Mechanistic investigations revealed that the expression of DSE altered CCL5 signaling and cell surface binding in HCC cells. Accordingly, DSE suppressed CCL5-induced cell growth, migration, and invasion, whereas silencing of DSE enhanced CCL5-triggered malignant phenotypes. Inhibiting CCR1 activity with BX471 decreased CCL5-induced malignant characters caused by siRNA-mediated knockdown of DSE in HCC cells, establishing the critical role of the CCL5/CCR1 axis in mediating the effects of DSE expression. Taken together, our results suggest that DSE dysregulation contributes to the malignant behavior of HCC cells. This provides novel insight into the significance of DSE in CCL5 signaling and HCC pathogenesis.
Indexed as
Identifiers
30906633PMC6405965W2980454391What OpenQuestion holds
Registered trials
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