| First Author | Hwang BJ | Year | 2019 |
| Journal | Oncogene | Volume | 38 |
| Issue | 50 | Pages | 7491-7503 |
| PubMed ID | 31435021 | Mgi Jnum | J:289734 |
| Mgi Id | MGI:6435456 | Doi | 10.1038/s41388-019-0961-9 |
| Citation | Hwang BJ, et al. (2019) The dysfunction of BP180/collagen XVII in keratinocytes promotes melanoma progression. Oncogene 38(50):7491-7503 |
| abstractText | BP180, also termed collagen XVII, is a hemidesmosomal transmembrane glycoprotein expressed in basal keratinocytes, and functions as a cell-matrix adhesion molecule in the dermal-epidermal junction of the skin. Its function, other than cell-matrix adhesion, remains unclear. We generated a mouse strain with BP180 dysfunction (termed NC16A), which develops spontaneous skin inflammation accompanied by an influx of myeloid derived suppressor cells (MDSCs). We used the B16 mouse melanoma model to demonstrate that BP180 dysfunction in either skin or basal keratinocytes promotes MDSC influx into skin and tumor progression. MDSC depletion reduced tumor progression in NC16A mice, demonstrating a critical role for BP180 dysfunction-driven MDSCs in melanoma progression. This study provides the first direct evidence that BP180, a cell-cell matrix adhesion molecule, possesses antitumor function through modulating infiltration of MDSCs. Basal keratinocytes actively participate in skin microenvironment changes caused by BP180 dysfunction. NC16A mice could be a new animal model to study the melanoma microenvironment. |
