Roles of Ras Homolog A in Invasive Ductal Breast Carcinoma

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  • Murakami Eriko
    Department of Breast Surgery, Nihon University School of Medicine
  • Nakanishi Yoko
    Department of Pathology, Nihon University School of Medicine
  • Hirotani Yukari
    Department of Pathology, Nihon University School of Medicine
  • Ohni Sumie
    Department of Pathology, Nihon University School of Medicine
  • Tang Xiaoyan
    Department of Pathology, Nihon University School of Medicine
  • Masuda Shinobu
    Department of Pathology, Nihon University School of Medicine
  • Enomoto Katsuhisa
    Department of Breast Surgery, Nihon University School of Medicine
  • Sakurai Kenichi
    Department of Breast Surgery, Nihon University School of Medicine
  • Amano Sadao
    Department of Breast Surgery, Nihon University School of Medicine
  • Yamada Tsutomu
    Department of Pathology, Nihon University School of Medicine
  • Nemoto Norimichi
    Department of Pathology, Nihon University School of Medicine Research Institute of Medical Science, Nihon University School of Medicine

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Abstract

<p>Breast cancer has a poor prognosis owing to tumor cell invasion and metastasis. Although Ras homolog (Rho) A is involved in tumor cell invasion, its role in breast carcinoma is unclear. Here, RhoA expression was examined in invasive ductal carcinoma (IDC), with a focus on its relationships with epidermal-mesenchymal transition (EMT) and collective cell invasion. Forty-four surgical IDC tissue samples and two normal breast tissue samples were obtained. RhoA, E-cadherin, vimentin, and F-actin protein expression were analyzed by immunohistochemistry. RhoA, ROCK, mTOR, AKT1, and PIK3CA mRNA expression were conducted using laser microdissection and semi-nested quantitative reverse transcription-polymerase chain reaction. RhoA expression was stronger on the tumor interface of IDCs than the tumor center (P<0.001). RhoA expression was correlated with ROCK expression only in HER2-subtype IDC (P<0.05). In IDCs co-expressing RhoA and ROCK, F-actin expression was stronger on the tumor interface, particularly at the edges of tumor cells, than it was in ROCK-negative IDCs (P<0.0001). In conclusion, RhoA expression was not correlated with EMT in IDC, but enhanced F-actin expression was localized on the edge of tumor cells that co-expressed ROCK. RhoA/ROCK signaling may be associated with collective cell invasion, particularly in HER2-subtype IDC.</p>

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