Rapamycin-induced G1 cell cycle arrest employs both TGF-β and Rb pathways. Issue 2 (1st May 2015)

• Record Type: Journal Article
• Authors: Chatterjee, Amrita; Mukhopadhyay, Suman; Tung, Kaity; Patel, Deven; Foster, David A.
• Is Part Of: Cancer letters. Volume 360:Issue 2(2015)
• Page Start: 134
• Page End: 140
• Publication Date: 2015-05-01
• Subjects: Cancer -- Periodicals; Neoplasms -- Periodicals; Cancer -- Périodiques; Electronic journals; 616.994
• DOI: 10.1016/j.canlet.2015.01.043
• Languages: English
• ISSNs: 0304-3835

Abstract

<abstract abstract-type="author-highlights" id="ab0010"> <title id="st0010">Highlights</title> <sec> <p id="sp0010"> <list id="ulist0010"> <list-item id="u0010"> <label></label> <p id="p0010">Rapamycin-induced G1 cell cycle arrest is dependent on TGF-β.</p> </list-item> <list-item id="u0015"> <label></label> <p id="p0015">Rapamycin-induced TGF-β signals requires nano-molar doses that suppress the phosphorylation of S6 kinase.</p> </list-item> <list-item id="u0020"> <label></label> <p id="p0020">Complete G1 arrest requires micro-molar doses of rapamycin that suppress phosphorylation of 4E-BP1.</p> </list-item> <list-item id="u0025"> <label></label> <p id="p0025">The effect of suppressing 4E-BP1 phosphorylation on G1 cell cycle progression is the inhibition of Rb phosphorylation.</p> </list-item> <list-item id="u0030"> <label></label> <p id="p0030">This study reveals the integration of TGF-β signals with Rb signals to promote complete G1 cell cycle progression.</p> </list-item> </list> </p> </sec> </abstract>