Nagoya University · Medicine
Professor Hiroaki Kajiyama's research lab focuses on the molecular mechanisms underlying peritoneal metastasis and drug resistance in epithelial ovarian carcinoma (EOC). The lab investigates key biological processes such as epithelial-mesenchymal transition (EMT), tumor-stroma interactions, and the role of signaling axes like SDF-1α/CXCR4 and cell surface enzymes such as DPPIV/CD26 in modulating cancer cell invasiveness and chemoresistance. Using in vitro, in vivo, and omics-based approaches, the lab explores how tumor cells interact with the peritoneal microenvironment—including mesothelial cells and plasma-activated media—to identify novel therapeutic targets for improving patient outcomes.
Figures are computed from collected data and may differ slightly.
The aim of this study was to assess paclitaxel resistant-epithelial ovarian carcinoma (EOC) cells for cellular morphology, motility, and molecular changes consistent with epithelial-mesenchymal transition (EMT). The human EOC cell lines NOS-2, TAOV and SKOV-3 were continuously exposed to increasing doses of paclitaxel to establish three stable cell lines resistant to paclitaxel (NOS-PR, TAOV-PR, and SKOV-PR cells, respectively). Using these cell lines, cellular functions such as motility, invasi
We demonstrated that plasma-activated medium also had an anti-tumor effect on chemo-resistant cells in vitro and in vivo. Indirect plasma therapy is a promising treatment option for EOC and may contribute to a better patient prognosis in the future.
Epithelial ovarian carcinoma (EOC) spreads by implantation of tumor cells onto the human peritoneal mesothelial cells (HPMCs) lining the peritoneal cavity. The aim of this study was to determine whether the stromal cell-derived factor-1alpha (SDF-1alpha)/CXCR4 axis is involved in the interaction of EOC cells with HPMCs in peritoneal metastasis. Clinically, we first evaluated CXCR4 expression in sections from 36 primary EOCs using immunohistochemistry. We next examined whether SDF-1alpha played r
Dipeptidyl peptidase IV (DPPIV) is a multifunctional cell surface aminopeptidase with ubiquitous expression. Recent studies have suggested that DPPIV plays an important role in tumor progression in several human malignancies. In the present study, we investigated the correlation between DPPIV expression and progressive potential in ovarian carcinoma. We demonstrated that ovarian carcinoma cell lines with higher DPPIV expression were less invasive. Furthermore, DPPIV overexpression in SKOV3 cells
Dipeptidyl peptidase IV (DPPIV/CD26) is a multifunctional cell surface aminopeptidase that is widely expressed in different cell types. Our previous study demonstrated a possible link between DPPIV expression and decreased i.p. dissemination and loss of invasive potential of ovarian carcinoma. In this report, we examined the mechanisms of the anti-invasive ability of DPPIV in greater detail. Expression of E-cadherin and beta-catenin was positively correlated with DPPIV expression among five inde
Peritoneal dissemination of ovarian cancer (OvCa) arises from the surface of the peritoneum, covered by monolayer of mesothelial cells (MCs). Given that both OvCa cells and MCs are present in the same peritoneal metastatic microenvironment, they may establish cell-to-cell crosstalk or phenotypic alterations including the acquisition of platinum-resistance in OvCa cells. Herein, we report how OvCa-associated mesothelial cells (OCAMs) induce platinum-resistance in OvCa cells through direct cell-to
Stage I EOC patients treated with FSS showed an acceptable prognosis compared with those who underwent RS.
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