Details

Autor(en) / Beteiligte

• Park, Hae-Min
• Hwang, Mintai Peter
• Kim, Yoon-Woo
• Kim, Kyoung-Jin
• Jin, Jang Mi
• Kim, Young Hwan
• Yang, Yung-Hun
• Lee, Kwan Hyi
• Kim, Yun-Gon

Titel

Mass spectrometry-based N-linked glycomic profiling as a means for tracking pancreatic cancer metastasis

Ist Teil von

• Carbohydrate research, 2015-09, Vol.413, p.5-11

Ort / Verlag

Netherlands: Elsevier Ltd

Erscheinungsjahr

2015

Quelle

MEDLINE

Beschreibungen/Notizen

• The aberrant glycosylation profile on the surface of cancer cells has been recognized for its potential diagnostic value towards assessing tumor progression. In this study, we initially investigate N-glycan profiles on the surface of normal (HPDE) and cancerous (Capan-1, Panc-1, and MIA PaCa-2) pancreatic cell lines, which are from different sites of pancreatic tumor. The enzymatically deglycosylated total N-glycans are permethylated via a quantitative solid-phase method and then analyzed by using MALDI-TOF MS and MALDI-QIT-TOF MS. We demonstrate that the level of high-mannose type glycans is higher among Capan-1 cells—pancreatic cancer cells that have metastasized to the liver—than that observed among Panc-1 and MIA PaCa-2 cells—pancreatic cancer cells from the pancreas duct head and tail regions, respectively. Furthermore, the relative abundance of highly-branched sialyted N-glycans is significantly up-regulated on Panc-1 and MIA PaCa-2 pancreatic cancer cells compared to that of normal HPDE pancreas cells. Taken together, these results indicate that specific N-glycosylation profile changes in pancreatic cancer cells can be used to not only distinguish between normal and cancerous cells but also provide more information on their location and metastatic potential. [Display omitted] •Total N-glycans are identified via quantitative mass spectrometric approaches.•The relative quantity of high-mannose glycans is higher on Capan-1 cancer cells.•The highly-branched sialyted N-glycans is up-regulated on Panc-1 and MIA PaCa-2.•N-glycosylation on pancreatic cancer cells depend on the site of tumor metastasis.