Yojiro Kotake1,2, Takeshi Tsuruda2. 1. Graduate School of Humanity-Oriented Science and Engineering, Kindai University, Fukuoka, Japan ykotake@fuk.kindai.ac.jp. 2. Department of Biological and Environmental Chemistry, Faculty of Humanity-Oriented Science and Engineering, Kindai University, Fukuoka, Japan.
Abstract
BACKGROUND/AIM: The INK4 locus encodes three important genes p15INK4B, p16INK4A, and ARF, which function to suppress oncogenesis, and a long noncoding RNA, ANRIL, which, in contrast, functions to promote oncogenesis. Herein, we report a fifth genetic element on the INK4 locus, a long noncoding RNA with unknown function named associated negative regulation of cell proliferation (ANROC), which played a role in the suppression of cell proliferation. MATERIALS AND METHODS: Following ANROC silencing in cells by siRNA, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and cell cycle analysis using flow cytometry were performed. RESULTS: ANROC expression was decreased by oncogenic RAS signalling. ANROC knockdown enhanced HeLa cell proliferation and induced cyclin B1 mRNA, which promotes G2/M progression of the cell cycle. Furthermore, flow cytometric analysis revealed that ANROC knockdown increased the percentage of cells in the S and G2/M phases of the cell cycle. CONCLUSION: ANROC functions to suppress cell cycle progression by suppressing cyclin B1 expression, thus inhibiting cell proliferation. Copyright
BACKGROUND/AIM: The INK4 locus encodes three important genes p15INK4B, p16INK4A, and ARF, which function to suppress oncogenesis, and a long noncoding RNA, ANRIL, which, in contrast, functions to promote oncogenesis. Herein, we report a fifth genetic element on the INK4 locus, a long noncoding RNA with unknown function named associated negative regulation of cell proliferation (ANROC), which played a role in the suppression of cell proliferation. MATERIALS AND METHODS: Following ANROC silencing in cells by siRNA, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and cell cycle analysis using flow cytometry were performed. RESULTS: ANROC expression was decreased by oncogenic RAS signalling. ANROC knockdown enhanced HeLa cell proliferation and induced cyclin B1 mRNA, which promotes G2/M progression of the cell cycle. Furthermore, flow cytometric analysis revealed that ANROC knockdown increased the percentage of cells in the S and G2/M phases of the cell cycle. CONCLUSION: ANROC functions to suppress cell cycle progression by suppressing cyclin B1 expression, thus inhibiting cell proliferation. Copyright
Authors: Kyoko L Yap; Side Li; Ana M Muñoz-Cabello; Selina Raguz; Lei Zeng; Shiraz Mujtaba; Jesús Gil; Martin J Walsh; Ming-Ming Zhou Journal: Mol Cell Date: 2010-06-11 Impact factor: 17.970
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