Transforming growth factor β1 contributes to the invasiveness of pancreatic ductal adenocarcinoma cells through the regulation of CD24 expression.

Objectives: The aim of this study was to investigate the role of CD24 in the invasiveness of pancreatic ductal adenocarcinoma (PDAC).

Methods: We used 2 human PDAC cell lines containing large numbers of CD24-positive (CD24) cells (>65%; AsPC-1 cells) or few CD24 cells (<20%; CFPAC-1 cells). Invasiveness was estimated using the Matrigel invasion assay.

Gamma-secretase complexes regulate the responses of human pancreatic ductal adenocarcinoma cells to taxanes.

Background/aim: It was previously reported that γ-secretase inhibitors (GSIs) enhance taxane-induced mitotic arrest and apoptosis in colon cancer cells. To enable the development of taxane-based chemotherapy for pancreatic ductal adenocarcinoma (PDAC), this study investigated the molecular mechanisms by which γ-secretase (GS) complexes regulate taxane sensitivity.

Materials And Methods: The effect of GS complexes on taxane-induced apoptosis in PDAC cells was evaluated by a cell cycle analysis.

Inhibition of Wnt signaling pathway decreases chemotherapy-resistant side-population colon cancer cells.

Background: The prognosis of advanced or recurrent colorectal cancer is still poor. Dye-effluxing side population (SP) colon cancer cells are reportedly resistant to chemotherapeutic agents. Most sporadic colorectal cancers involve constitutive activation of the Wnt signaling pathway.

Intratumoral CD8(+) T/FOXP3 (+) cell ratio is a predictive marker for survival in patients with colorectal cancer.

The human immune system consists of a balance between immune surveillance against non-self antigens and tolerance of self-antigens. CD8(+) T cells and CD4(+) regulatory T cells (Tregs) are the main players for immune surveillance and tolerance, respectively. We examined immunohistochemically the immunological balance at the tumor site using 94 surgically resected colorectal cancer tissues.

Nuclear factor kappaB-activated monocytes contribute to pancreatic cancer progression through the production of Shh.

Recently, it was reported that Hh signaling is activated in tumor stromal cells but not in tumor cells themselves and that stromal cells may play a role in the proliferation of cancer cells. This suggests the possibility that stromal cells have an important role in the proliferation of tumor cells that may be mediated through Hh signaling. In this report, we present for the first time that inflammation-stimulated monocytes produce Shh through activation of the NF-kappaB signaling pathway, and that the Shh produced promotes the proliferation of pancreatic cancer cells in a paracrine manner through Hh signaling.

A protein-bound polysaccharide, PSK, enhances tumor suppression induced by docetaxel in a gastric cancer xenograft model.

Background: We have reported previously that docetaxel (TXT) induces apoptosis and nuclear factor-kappaB (NF-kappaB) activation, and that blockade of NF-kappaB activation augments TXT-induced apoptosis in human gastric cancer cells. In addition, we have also shown that a protein-bound polysaccharide PSK enhances TXT-induced apoptosis through NF-kappaB inhibition in human pancreatic cancer cells. Based on these observations, in the present study the possibility that PSK could enhance TXT-mediated tumor suppression was examined in vivo and in vitro.