Antiprotease in preventing the invasive potential of pancreatic cancer cells

Hiroki Takahashi, Hirozumi Sawai, Hitoshi Funahashi, Yoichi Matsuo, Akira Yasuda, Nobuo Ochi, Mikinori Sato, Yuji Okada, Hiromitsu Takeyama

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

Abstract

The process of tumor progression and metastasis involves degradation of the extracellular matrix and is governed by an intricate balance of proteases, their activators and their inhibitors, in which malignant cells are permitted to infiltrate the adjacent structures and gain access to lymph and blood vessels. These proteases can be broadly categorized into three families: matrix metalloproteinases, serine proteinases and cysteine proteinases, all of which have all been implicated in these processes. The presence of neural invasion is often considered to be a poor prognostic sign; however, the cellular mechanisms underlying this propensity for perineural invasion are unknown. We recently researched the relationship between the glial cell line-derived neurotrophic factor and perineural invasion by human pancreatic cancer cells. We also confirmed that NF-kappa B is a part of the signaling pathway from the glial cell line-derived neurotrophic factor in human pancreatic cancer cells, and documented the inhibitory effect of gabexate mesilate, a well-known non-physiological synthetic serine protease inhibitor, for pancreatic cancer invasion. Recent studies on the role of proteases and protease inhibitors in pancreatic cancer invasion are also reviewed.

Original languageEnglish
Pages (from-to)501-508
Number of pages8
JournalJournal of the Pancreas
Volume8
Issue number4
Publication statusPublished - 01-07-2007
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Hepatology
  • Endocrinology

Fingerprint

Dive into the research topics of 'Antiprotease in preventing the invasive potential of pancreatic cancer cells'. Together they form a unique fingerprint.

Cite this