A novel ameloblastoma cell line (AM-3) secretes MMP-9 in response to Wnt-3a and induces osteoclastogenesis

Kibe, Toshiro; Fuchigami, Takao; Kishida, Michiko; Iijima, Mikio; Ishihata, Kiyohide; Hara, Hiroshi; Miyawaki, Akihiko; Semba, Ichiro; Nakamura, Norifumi; Kiyono, Tohru; Kishida, Shosei

doi:10.1016/j.oooo.2013.03.005

Cited by 27 publications

(40 citation statements)

References 38 publications

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“…In hTERT + ‐AM cells, MMP‐2 and MMP‐9 were upregulated under elevated HP, consistent with a previous study on osteocytes . Wnt signalling is known to induce MMP‐9 in ameloblastoma cells . In hTERT + ‐AM cells, when Wnt signalling was blocked, HP‐induced upregulation of MMPs was abolished.…”

Section: Discussionsupporting

confidence: 90%

Elevated hydrostatic pressure promotes ameloblastoma cell invasion through upregulation of MMP‐2 and MMP‐9 expression via Wnt/β‐catenin signalling

Yang

Liang

et al. 2018

J Oral Pathology Medicine

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This study indicates that elevated hydrostatic pressure promotes the migration and invasion of ameloblastoma cells by activating the Wnt/β-catenin pathway, thereby increasing expression of MMP-2, MMP-9 and other Wnt signalling downstream targets. This suggests that marsupialization may reduce invasiveness and reverse the bone resorption process by lowering intracystic hydrostatic pressure in cystic ameloblastoma.

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Section: Discussionsupporting

confidence: 90%

Elevated hydrostatic pressure promotes ameloblastoma cell invasion through upregulation of MMP‐2 and MMP‐9 expression via Wnt/β‐catenin signalling

Yang

Liang

et al. 2018

J Oral Pathology Medicine

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“…Previously, we investigated differences in gene expression on several factors associated with cellular invasion in the past study. For example, the expressions of MMP series such as MMP‐9, which is a digestive protease, are different between AM‐1 and AM‐3 cells . In that study, we have shown that Wnt‐3a promotes the expression of MMP‐9 from ameloblastoma cells.…”

Section: Discussionmentioning

confidence: 99%

“…Other group reported that the gene mutations such as SMO and BRAF existed in ameloblastoma and that the mutation pattern differed between plexiform type and follicular type . We have shown that different types of ameloblastoma cells have characteristic properties in gene expression pattern and invasion activity . Based on these findings, we hypothesized that intercellular interactions between ameloblastoma cells and the neighboring stroma could also affect the collective invasion of ameloblastoma cells.…”

mentioning

confidence: 99%

Fibroblasts promote the collective invasion of ameloblastoma tumor cells in a 3D coculture model

et al. 2017

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Ameloblastoma is a benign tumor of the odontogenic epithelium with several histological subtypes. All subtypes of ameloblastoma contain abundant stroma; the tumor cells invade collectively into the surrounding tissues without losing intratumor cell attachments. However, the molecular mechanisms mediating ameloblastoma invasion remain unclear. Here, we evaluated the functional significance of the interactions between ameloblastoma tumor cells and stromal fibroblasts on collective cellular invasion using a three‐dimensional cultivation method, double‐layered collagen gel hemisphere ( DL ‐ CGH ) culture. The AM ‐1 plexiform and AM ‐3 follicular human ameloblastoma cell lines and HFF ‐2 human fibroblasts were labeled with GFP and DsRed, respectively. Collective cellular invasion of ameloblastoma cells was assessed in the presence or absence of fibroblasts. Notably, without fibroblasts, AM ‐1 cells formed sharp, plexiform‐like invasive processes, whereas AM ‐3 cells formed a series of blunt processes often observed during collective migration. In comparison, under the cocultures with HFF ‐2 fibroblasts, AM ‐3 cells formed tuft‐like invasive processes and collectively invaded into outer layer more than that observed with AM ‐1 cells. Moreover, HFF ‐2 fibroblasts localized to the tips of the invasive tumor processes. These findings suggest that tumor‐associated cells assist tumor cell invasion. Microscopic analysis of sectioned three‐dimensional cultures revealed that AM ‐3/ HFF ‐2 hemispheres were histologically similar to follicular ameloblastoma tumor samples. Therefore, our findings suggest that ameloblastoma subtypes exhibit distinct invasion patterns and that fibroblasts promote collective tumor invasion in follicular ameloblastoma.

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“…Another study used two immortalized ameloblastoma cell lines (AM-1 and AM-3) to evaluate the expression of Wnt ligands and receptors and the effects of Wnt-3a expression [78]. They showed that AM-1, AM-3, and MOE1b (normal oral epithelium) cells expressed mRNA for both canonical and non-canonical Wnt ligands (Wnt2, 2B, 4, 5A, 5B, 7B, 8B, 9B, and 11) and Wnt receptors (Frizzled1, 2, 3, 4, 5, 6, 7, 8, 9, 10, LRP5, LRP6).…”

Section: Wntmentioning

confidence: 99%

Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis

Amm

MacDougall

2016

Curr Oral Health Rep

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Several molecular pathways have been shown to play critical roles in the pathogenesis of odontogenic tumors. These neoplasms arise from the epithelial or mesenchymal cells of the dental apparatus in the jaw or oral mucosa. Next generation genomic sequencing has identified gene mutations or single nucleotide polymorphisms associated with many of these tumors. In this review, we focus on two of the most common odontogenic tumor subtypes: ameloblastoma and keratocystic odontogenic tumors. We highlight gene expression and protein immunohistological findings and known genetic alterations in the hedgehog, BRAF/Ras/MAPK, epidermal growth factor receptor, Wnt and Akt signaling pathways relevant to these tumors. These various pathways are explored to potentially target odontogenic tumors cells and prevent growth and recurrence of disease. Through an understanding of these signaling pathways and their crosstalk, molecular diagnostics may emerge as well as the ability to exploit identified molecular differences to develop novel molecular therapeutics for the treatment of odontogenic tumors.

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A novel ameloblastoma cell line (AM-3) secretes MMP-9 in response to Wnt-3a and induces osteoclastogenesis

Cited by 27 publications

References 38 publications

Elevated hydrostatic pressure promotes ameloblastoma cell invasion through upregulation of MMP‐2 and MMP‐9 expression via Wnt/β‐catenin signalling

Elevated hydrostatic pressure promotes ameloblastoma cell invasion through upregulation of MMP‐2 and MMP‐9 expression via Wnt/β‐catenin signalling

Fibroblasts promote the collective invasion of ameloblastoma tumor cells in a 3D coculture model

Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis

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