To control in invasion and metastasis through EMT (Epithelial-Mesenchymal-Transition) functional analysis of CD24 in endometrial cancer

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390384
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Osaka Medical College
• Principal Investigator: OHMICHI Masahide 大阪医科大学, 医学部, 教授 (10283764)
• Co-Investigator(Kenkyū-buntansha): TANABE Akiko 大阪医科大学, 医学部, 非常勤講師 (70454543) ; HAYASHI Masami 大阪医科大学, 医学部, 講師 (00551748) ; TANAKA Yoshimichi 大阪医科大学, 医学部, 助教 (10625502) ; KANEMURA Masanori 大阪医科大学, 医学部, 講師 (40298782) ; YAMASHITA Yoshiki 大阪医科大学, 医学部, 非常勤講師 (50268207) ; TSUNETOH Satoshi 大阪医科大学, 医学部, 助教 (70388255) ; TERAI Yoshito 大阪医科大学, 医学部, 准教授 (90278531)
• Research Collaborator: NAKAMURA Kiyoko 大阪医科大学, 医学部
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 子宮内膜癌 / EMT / CD24 / HGF / Met / ABC transporter

Outline of Final Research Achievements

The development of resistance to chemotherapeutic drugs by cancer cells represents a major challenge in the clinical cure of advanced and metastatic cancers. CD24 has been reported to be a marker for a poor prognosis in several tumors, and we herein examined the functions of CD24 in human endometrioid adenocarcinoma cell lines, and evaluated how it contributes to cancer drug resistance. We demonstrated that CD24 was responsible for the recruitment of phosphorylated-Met to the lipid raft domain of the cell membrane, resulting in amplification of the Met signaling cascade, ultimately leading endometrial cancer cells to express higher levels of ATP binding cassette (ABC) transporters. Our findings suggest that CD24-mediated amplification of the Met cascade may contribute to the drug resistance of endometrial cancer.

Free Research Field

婦人科腫瘍学