title: SIRPalpha1 and SIRPalpha2: their role as tumor suppressors in breast carcinoma cells.
abstract: We have previously reported that expression of SIRPalpha1/SHPS-1 was strongly suppressed in v-Src-transformed cells and its forced expression resulted in the suppression of anchorage-independent growth of the cells [K. Machida, S. Matsuda, K. Yamaki, T. Senga, A.A. Thant, H. Kurata, K. Miyazaki, K. Hayashi, T. Okuda, T. Kitamura, T. Hayakawa, M. Hamaguchi, v-Src suppresses SHPS-1 expression via the Ras-MAP kinase pathway to promote the oncogenic growth of cells, Oncogene 19 (2000) 1710-1718]. We examined the effect of human SIRPalpha1 expression in breast cancer cell lines, Hs578T and MCF7, and compared with the effect of SIRPalpha2 expression in Hs578T. Forced expression of either SIRPalpha1 or SIRPalpha2 did not perturb the growth of Hs578T in a conventional attached condition. Their expression, however, enforced the actin stress fiber formation and induced activation of Rho, but not Rac, in Hs578T cells. Moreover, forced expression of either SIRPalpha1 or SIRPalpha2 displayed distinct suppressive effect on the anchorage-independent growth of Hs578T cells. Similarly, forced expression of SIRPalpha1 in MCF7 specifically suppressed the anchorage-independent growth of the cells. Taken together, our results strongly suggest the function of SIRPalpha1 and 2 as type II tumor suppressors for human breast carcinoma.
authors.affiliation: Division of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Yamasaki
authors.forename: Satoko
authors.initials: S
authors.lastname: Ito
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Tsunoda
authors.forename: Toshio
authors.initials: T
authors.lastname: Kokuryo
authors.forename: Kazuo
authors.initials: K
authors.lastname: Hara
authors.forename: Takeshi
authors.initials: T
authors.lastname: Senga
authors.forename: Reiji
authors.initials: R
authors.lastname: Kannagi
authors.forename: Tatsuyoshi
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Koji
authors.initials: K
authors.lastname: Oda
authors.forename: Masato
authors.initials: M
authors.lastname: Nagino
authors.forename: Yuji
authors.initials: Y
authors.lastname: Nimura
authors.forename: Michinari
authors.initials: M
authors.lastname: Hamaguchi
mesh_terms: D000595:Amino Acid Sequence; D000943:Antigens, Differentiation / Q000737:chemistry / Q000502:physiology*; D001940:Breast / Q000378:metabolism* / Q000473:pathology; D002277:Carcinoma / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D006801:Humans; D008969:Molecular Sequence Data; D011971:Receptors, Immunologic / Q000737:chemistry / Q000502:physiology*; D022502:Stress Fibers / Q000648:ultrastructure; D025521:Tumor Suppressor Proteins / Q000737:chemistry / Q000502:physiology*
chemical_list: D000943:Antigens, Differentiation; D011971:Receptors, Immunologic; C501920:SIRPA protein, human; D025521:Tumor Suppressor Proteins