Roudy Chiminch Ekyalongo1, Toru Mukohara2, Yohei Funakoshi1, Hideo Tomioka1, Yu Kataoka1, Yohei Shimono3, Naoko Chayahara1, Masanori Toyoda1, Naomi Kiyota1, Hironobu Minami4. 1. Division of Medical Oncology/Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Kobe, Japan. 2. Division of Medical Oncology/Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Kobe, Japan Cancer Center, Kobe University Hospital, Kobe, Japan mukohara@med.kobe-u.ac.jp. 3. Division of Medical Oncology/Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Kobe, Japan Division of Molecular and Cellular Biology, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Japan. 4. Division of Medical Oncology/Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Kobe, Japan Cancer Center, Kobe University Hospital, Kobe, Japan.
Abstract
AIM: We evaluated the potential of TYRO3 as a therapeutic target in various types of breast cancer cell lines. MATERIALS AND METHODS: The effects of TYRO3-knockdown by small interfering RNA (siRNA) on proliferation, cell-cycle distribution, and cell signaling in four estrogen receptor (ER)-positive/HER2-non-amplified (luminal-type), two ER-negative/HER2-amplified (HER2-type), and two ER-negative/HER2-non-amplified (triple negative [TN]-type) cell lines were compared. RESULTS: Whereas TYRO3 knockdown induced the greatest proliferation suppression in luminal-type cells, and to a lesser extent in HER2-type cells, no proliferation inhibition was observed in TN-type cells. The TYRO3 siRNA-induced proliferation inhibition in luminal-type cells was observed in both estradiol (E2)-rich and -null conditions. The proliferation suppression was correlated with G0-G1/S cell-cycle arrest. Western blot analysis showed a decrease in phosphorylation of ERK1/2 or STAT3, and in cyclin D1 only in cell lines sensitive to TYRO3-knockdown. CONCLUSION: TYRO3 is a potential therapeutic target in breast cancer, particularly in luminal-type cells. Copyright
AIM: We evaluated the potential of TYRO3 as a therapeutic target in various types of breast cancer cell lines. MATERIALS AND METHODS: The effects of TYRO3-knockdown by small interfering RNA (siRNA) on proliferation, cell-cycle distribution, and cell signaling in four estrogen receptor (ER)-positive/HER2-non-amplified (luminal-type), two ER-negative/HER2-amplified (HER2-type), and two ER-negative/HER2-non-amplified (triple negative [TN]-type) cell lines were compared. RESULTS: Whereas TYRO3 knockdown induced the greatest proliferation suppression in luminal-type cells, and to a lesser extent in HER2-type cells, no proliferation inhibition was observed in TN-type cells. The TYRO3 siRNA-induced proliferation inhibition in luminal-type cells was observed in both estradiol (E2)-rich and -null conditions. The proliferation suppression was correlated with G0-G1/S cell-cycle arrest. Western blot analysis showed a decrease in phosphorylation of ERK1/2 or STAT3, and in cyclin D1 only in cell lines sensitive to TYRO3-knockdown. CONCLUSION:TYRO3 is a potential therapeutic target in breast cancer, particularly in luminal-type cells. Copyright
Authors: Zhifen Zhou; Min Li; Lin Zhang; Hong Zhao; Özgür Şahin; Jing Chen; Jean J Zhao; Zhou Songyang; Dihua Yu Journal: Cancer Res Date: 2018-02-12 Impact factor: 12.701
Authors: Robin Schmitz; Aida Freire Valls; Rosario Yerbes; Sophie von Richter; Christoph Kahlert; Sonja Loges; Jürgen Weitz; Martin Schneider; Carmen Ruiz de Almodovar; Alexis Ulrich; Thomas Schmidt Journal: Oncotarget Date: 2016-08-30