Role of the cell polarity regulator aPKC in uterine cervical cancer and cervical intraepithelial lesion.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10725
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Yokohama City University
• Principal Investigator: MARUYAMA Yasuyo 横浜市立大学, 医学研究科, 共同研究員 (10534141)
• Co-Investigator(Kenkyū-buntansha): 長嶋 洋治 東京女子医科大学, 医学部, 教授 (10217995) ; 秋本 和憲 東京理科大学, 薬学部生命創薬科学科, 准教授 (70285104)
• Co-Investigator(Renkei-kenkyūsha): MIYAGI Etsuko 横浜市立大学, 医学研究科, 教授 (40275053) ; SATO Mikiko 横浜市立大学, 大学病院, 准教授 (70326049) ; HIRAHARA Fumiki 国立病院機構, 横浜医療センター, 院長 (30201734)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: aPKC / 子宮頸がん / 子宮頸部異形成

Outline of Final Research Achievements

The aim of the study was to explore the role of aPKC, a cell polarity regulator as well as a oncogene, in development and progression of cervical cancer. For this purpose, the expression patterns of aPKC were assessed in cervical cancer and its precursor lesion (SIL).
In a part of cervical cancer and SIL, aPKC over-expressed or aberrantly located in nucleus. The prognoses of the cervical cancer patients with nuclear aPKC were significantly poorer than the patients with cytoplasmic aPKC. Furthermore, over-expression of aPKC and nuclear localization in low grade SIL were risk factor of progression to higher grade of SIL. In addition, cervical cancer cell lines with forced expression of aPKC in nucleus showed higher invasive capacity than aPKC knock-down cells.
Our study suggested the implication of aPKC in oncogenesis and progression of cervical squamous carcinoma.

Free Research Field

産婦人科