<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">KOTAKE, YOJIRO</style></author><author><style face="normal" font="default" size="100%">TSURUDA, TAKESHI</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Long Noncoding RNA &lt;em&gt;ANROC&lt;/em&gt; on the &lt;em&gt;INK4&lt;/em&gt; Locus Functions to Suppress Cell Proliferation</style></title><secondary-title><style face="normal" font="default" size="100%">Cancer Genomics - Proteomics</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2020</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2020-07-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">425-430</style></pages><doi><style  face="normal" font="default" size="100%">10.21873/cgp.20201</style></doi><volume><style face="normal" font="default" size="100%">17</style></volume><issue><style face="normal" font="default" size="100%">4</style></issue><abstract><style  face="normal" font="default" size="100%">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.</style></abstract></record></records></xml>