N-Glycosylation Induces the CTHRC1 Protein and Drives Oral Cancer Cell Migration

Liu, Gangli; Sengupta, Pritam K.; Jamal, Basem T.; Yang, Hsiao-Ying; Bouchie, Meghan P.; Lindner, Volkhard; Varelas, Xaralabos; Kukuruzinska, Maria A.

doi:10.1074/jbc.m113.473785

Cited by 66 publications

(82 citation statements)

References 42 publications

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“…In the presence of ligand Wnt3a/1/8, Wnt/β-catenin pathway will be activated, including Wnt-FZDs-Lrp5/6 complex which transduces signals to the cellular downstream and leads to accumulation of β-catenin in cytoplasm. The upregulated β-catenin translocates to nucleus and regulates a wide range of genes by binding to a series transcription factors such as TCF/LEF 20. There is scientific evidence suggesting that the biological effect of CTHRC1 on metastasis and proliferation of tumor cells is cross-linked with the canonical Wnt/β-catenin pathway.…”

Section: The Role Of Cthrc1 In Multi-signaling Pathwaysmentioning

confidence: 99%

“…Excavated molecular biology characterizations reveal that the expression level of CTHRC1 significantly correlates with transforming growth factor-β (TGF-β1) and promoter demethylation 13, 19. Furthermore, N-glycosylation may cooperate with canonical Wnt signaling pathways to intensify the overexpression of CTHRC1 and promote Oral squamous cell carcinoma (OSCC) metastasis 20.…”

Section: Introductionmentioning

confidence: 99%

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Multidimensional Roles of Collagen Triple Helix Repeat Containing 1 (CTHRC1) in Malignant Cancers

et al. 2016

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Tumor is one of the principal diseases that seriously threaten human health. Insight into sensitive cancer markers may open a new avenue for the early diagnosis and treatment of this disease. CTHRC1 has been identified as a cancer-related gene. It is a secretory glycoprotein that possesses multidimensional roles associated with wound repair, bone remodeling, hepatocytes fibrosis, adipose tissue formation, and so on. Our previous studies and numerous reports from other researchers have revealed that the ascended expression of CTHRC1 tends to go hand in hand with tumorigenesis, proliferation, invasion and metastasis in various human malignancies through a series of molecular mechanisms and signaling pathways. However, the detailed pathogenic mechanisms of CTHRC1 overexpression in human malignant cancers are not yet clear. Here, we shall focus our description on the functions, expression profile in several representative malignant tumors and a number of molecular mechanisms and signaling pathways involved with CTHRC1. This introductory discussion of CTHRC1 will serve as a reference for further research in understanding this intriguing cancer-related protein.

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Section: The Role Of Cthrc1 In Multi-signaling Pathwaysmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Multidimensional Roles of Collagen Triple Helix Repeat Containing 1 (CTHRC1) in Malignant Cancers

et al. 2016

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“…Atypical glycosylation of cell surface carbohydrates has been reported to be associated with malignant transformation of oral epithelium (9), and protein-bound sugar levels were higher in plasma and tissue samples of oral cancer patients (10). A series of studies about dysregulation of the N-glycosylation-regulating gene, DPAGT1, drives oral cancer cell discohesion by inhibiting adhesion of E-cadherin through Wnt signaling pathway were reported (11)(12)(13). It was also found that the expression of Lewis y on EGFR promotes migration of oral cancer cells (14).…”

mentioning

confidence: 99%

Glycoprotein B7-H3 overexpression and aberrant glycosylation in oral cancer and immune response

Chen

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

108

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The incidence and mortality rate of oral cancer continue to rise, partly due to the lack of effective early diagnosis and increasing environmental exposure to cancer-causing agents. To identify new markers for oral cancer, we used a sialylation probe to investigate the glycoproteins differentially expressed on oral cancer cells. Of the glycoproteins identified, B7 Homolog 3 (B7-H3) was significantly overexpressed in oral squamous cell carcinoma (OSCC), and its overexpression correlated with larger tumor size, advanced clinical stage, and low survival rate in OSCC patients. In addition, knockdown of B7-H3 suppressed tumor cell proliferation, and restoration of B7-H3 expression enhanced tumor growth. It was also found that the N-glycans of B7-H3 from Ca9-22 oral cancer cells contain the terminal α-galactose and are more diverse with higher fucosylation and better interaction with DC-SIGN [DC-specific intercellular adhesion molecule-3 (ICAM-3)-grabbing nonintegrin] and Langerin on immune cells than that from normal cells, suggesting that the glycans on B7-H3 may also play an important role in the disease.CD276 | proliferation | glycan sequencing | terminal α-galactose | fucose

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“…Furthermore, abnormal glycosylation of cell surface proteins takes place during which normal cells progress to a malignant neoplastic state [1]. Thus, the modification of cell surface glycosylation is a characteristic of many cancer cells [2–4]. Many of the recently developed tumor markers are carbohydrate antigens.…”

mentioning

confidence: 99%

Inhibition of N-Glycosylation towards Novel Anti-Cancer Chemotherapeutics

Kurosu¹

2018

J Mol Pharm Org Process Res

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N-Glycosylation Induces the CTHRC1 Protein and Drives Oral Cancer Cell Migration

Cited by 66 publications

References 42 publications

Multidimensional Roles of Collagen Triple Helix Repeat Containing 1 (CTHRC1) in Malignant Cancers

Multidimensional Roles of Collagen Triple Helix Repeat Containing 1 (CTHRC1) in Malignant Cancers

Glycoprotein B7-H3 overexpression and aberrant glycosylation in oral cancer and immune response

Inhibition of N-Glycosylation towards Novel Anti-Cancer Chemotherapeutics

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