TY - JOUR
T1 - Amurubicinol-induced eotaxin-3 expression in human NCI-H69 small cell lung carcinoma cells
AU - Niiya, Masami
AU - Niiya, Kenji
AU - Shibakura, Misako
AU - Asaumi, Noboru
AU - Yoshida, Chikamasa
AU - Tanimoto, Mitsune
PY - 2006/3
Y1 - 2006/3
N2 - We previously demonstrated the doxorubicin-induced expression of urokinase-type plasminogen activator (uPA), interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-α in human RCK8 lymphoma cells and NCI-H69 small cell lung carcinoma cells in which reactive oxygen species might be involved. Amurubicin hydrochloride (AMR), a novel derivative drug of doxorubicin, was recently introduced to clinical practice for treatment of lung cancer in Japan. Therefore, we investigated the effects of AMR on the expression of uPA and chemokines in NCI-H69 cells. AMR and its active form, amurubicinol hydrochloride (AMROH), both induced the expression of uPA, IL-8 and MCP-1 in H69 cells in a dose-dependent manner. When the cultured supernatant obtained from AMRtreated H69 cells was subcutaneously injected into rabbits, migration of a significant number of eosinophils was observed around the injected site. Antigen levels of eotaxin-3, a major migration-factor of eosinophils, were increased in AMROH-treated cells in parallel with the mRNA levels. The induction was observed below the clinically achievable concentration of AMR or AMROH. Thus, the simultaneous induction of uPA, IL-8, MCP-1 and eotaxin-3 may play a role in the pharmacological action of AMR through induction of the interaction between proinflammatory cells and lung carcinoma cells.
AB - We previously demonstrated the doxorubicin-induced expression of urokinase-type plasminogen activator (uPA), interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-α in human RCK8 lymphoma cells and NCI-H69 small cell lung carcinoma cells in which reactive oxygen species might be involved. Amurubicin hydrochloride (AMR), a novel derivative drug of doxorubicin, was recently introduced to clinical practice for treatment of lung cancer in Japan. Therefore, we investigated the effects of AMR on the expression of uPA and chemokines in NCI-H69 cells. AMR and its active form, amurubicinol hydrochloride (AMROH), both induced the expression of uPA, IL-8 and MCP-1 in H69 cells in a dose-dependent manner. When the cultured supernatant obtained from AMRtreated H69 cells was subcutaneously injected into rabbits, migration of a significant number of eosinophils was observed around the injected site. Antigen levels of eotaxin-3, a major migration-factor of eosinophils, were increased in AMROH-treated cells in parallel with the mRNA levels. The induction was observed below the clinically achievable concentration of AMR or AMROH. Thus, the simultaneous induction of uPA, IL-8, MCP-1 and eotaxin-3 may play a role in the pharmacological action of AMR through induction of the interaction between proinflammatory cells and lung carcinoma cells.
KW - Amurubicin
KW - Amurubicinol
KW - Eotaxin-3
KW - Interleukin-8
KW - Monocyte chemoattractant protein-1
KW - Small cell lung carcinoma cells
KW - Urokinase-type plasminogen activator
UR - http://www.scopus.com/inward/record.url?scp=33645731833&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33645731833&partnerID=8YFLogxK
U2 - 10.3892/or.15.3.571
DO - 10.3892/or.15.3.571
M3 - Article
C2 - 16465414
AN - SCOPUS:33645731833
SN - 1021-335X
VL - 15
SP - 571
EP - 576
JO - Oncology reports
JF - Oncology reports
IS - 3
ER -
