p62 Regulates the Proliferation of Molecular Apocrine Breast Cancer Cells

• Nozaki Fumi

  Department of Pathology, St. Luke’s International Hospital Department of Oncologic Pathology, Nihon University School of Medicine

• Hirotani Yukari

  Division of Morphological and Functional Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine

• Nakanishi Yoko

  Department of Oncologic Pathology, Nihon University School of Medicine

• Yamaguchi Hiromi

  Division of Morphological and Functional Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine

• Nishimaki Haruna

  Department of Oncologic Pathology, Nihon University School of Medicine

• Noda Hiroko

  Department of Oncologic Pathology, Nihon University School of Medicine

• Tang Xiaoyan

  Department of Oncologic Pathology, Nihon University School of Medicine

• Yamamoto Hisae

  Division of Pathology, Nihon University Itabashi Hospital

• Suzuki Atsuko

  Division of Pathology, Nihon University Itabashi Hospital

• Seki Toshimi

  Division of Pathology, Nihon University Itabashi Hospital

• Masuda Shinobu

  Department of Oncologic Pathology, Nihon University School of Medicine

Abstract

p62, also called sequestosome 1 (SQSTM1), is a multifunctional signaling molecule that affects cell proliferation. Recently, we found accumulation of p62 in apocrine carcinoma of the breast, however, the biological role of p62 expression in apocrine carcinoma still remains unclear. To investigate whether p62 might contribute to tumor cell proliferation in apocrine carcinomas, we used the MDA-MB-453 (androgen receptor-positive, HER2-type) and MFM223 (androgen receptor-positive, triple-negative type) breast cancer cell lines as models of molecular apocrine carcinoma. Both MDA-MB-453 and MFM223 showed strong and d high p62 protein expression than MCF7 cells (androgen receptor-negative, luminal A type). Knockdown of p62 resulted in significant reduction of the cell proliferative activity in both MDA-MB-453 (P<0.01) and MFM223 (P<0.05). In conclusion, p62 could contribute to cell proliferation and represent a therapeutic target in apocrine carcinoma.

Journal

• ACTA HISTOCHEMICA ET CYTOCHEMICA

  ACTA HISTOCHEMICA ET CYTOCHEMICA 49 (4), 125-130, 2016

  JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY

Keywords

• p62
• apocrine carcinoma
• breast cancer

Details

• CRID: 1390001204860810880
• NII Article ID: 130005262537
• DOI: 10.1267/ahc.16013
• ISSN: 13475800
• ISSN: 00445991
• Web Site: https://www.jstage.jst.go.jp/article/ahc/49/4/49_16013/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2017326413
• Text Lang: en
• Data Source:
  • JaLC
  • Crossref
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed