Deregulated c-myc expression in quiescent CHO cells induces target gene transcription and subsequent apoptotic phenotype

Abstract

Human c-myc cDNA was fused with the hormone-binding domain (HBD) cDNA of murine estrogen receptor gene and the chimeric gene was introduced into the CHO cells. The fusion protein, c-MycER, becomes activated when the synthetic steroid, 4-hydroxy-tamoxifen (OHT), binds HBD. Activated cMycER, likely c-Myc, can induce quiescent CHO cells reentry into S phase and subsequent cell death under serum-free condition. In addition, the expression of some proposed c-myc target genes such as ODC, MrDb, cad, rcc1 and rcl were found to increase upon OHT induction before S phase entry and apoptosis, indicating that these target genes are involved in cell cycle regulation and/or apoptosis control. However, the mutant D106-143c-MycER protein does not have above activities.

The E1∧E4 Protein of Human Papillomavirus Type 16 Associates with a Putative RNA Helicase through Sequences in Its C Terminus

“…Like SrmB, DeaD, and RhlB, the human Ddx1 protein also shared homology with E4-DBP in its Nterminal extension. Ddx1 and MrDb are frequently upregulated along with myc in human cancers and are thought to confer a proliferative advantage to cells (1,26,37). Only one protein showed homology with E4-DBP throughout its length (Caenorhabditis elegans protein; GenBank accession number Z29115) (Fig.…”

“…With the exception of eIF4A, which is involved in unwinding mRNAs at their 5Ј ends (64), the roles of most DEAD box proteins are poorly defined. Several have been found to affect cell proliferation (1,10,26,27,37,60,72), although in most cases, the direct effect on RNA processing which gives rise to this phenotype is not known. Among proteins with known functions, E4-DBP shares the greatest homology with Rrp3 (55) in its central domain and with the E. coli DEAD box protein SrmB (43) in its N-terminal extension.…”

Mitotic Functions of the Ran GTPase Network: the Importance of Being in the Right Place at the Right Time

“…74 RCC1 can also be aberrantly expressed in certain tumors, since the coding gene is a transcriptional target of the c-myc proto-oncogene 75 and is actually found to be deregulated in model cell lines overexpressing myc family members. 70,76,77 Thus, Ran network members, and particularly RanBP1 show altered expression in several types of tumors, and, conversely, are targeted by independent anti-cancer therapeuthical approaches. How might deregulation of Ran network components impact on mitotic division and genetic stability in mammalian cells?…”

Effect of heparin on apoptosis in human nasopharyngeal carcinoma CNE2 cells

“…The c-myc-me-diated apoptosis could be suppressed by cytokines such as platelet-derived growth factor (PDGF), insulin-like growth factor-I (IGF-I), and bcl-2. [16][17][18][19]. The c-myc promoter is characteristic of uniquely showing both RNA polymerase II (pol II) and RNA polymerase III (pol III) activities.…”