ORCID Profile
0000-0002-5671-1878
Current Organisation
Duke University
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Publisher: American Association for Cancer Research (AACR)
Date: 09-2013
DOI: 10.1158/2159-8290.CD-12-0592
Abstract: 3q26 is frequently lified in several cancer types with a common lified region containing 20 genes. To identify cancer driver genes in this region, we interrogated the function of each of these genes by loss- and gain-of-function genetic screens. Specifically, we found that TLOC1 (SEC62) was selectively required for the proliferation of cell lines with 3q26 lification. Increased TLOC1 expression induced anchorage-independent growth, and a second 3q26 gene, SKIL (SNON), facilitated cell invasion in immortalized human mammary epithelial cells. Expression of both TLOC1 and SKIL induced subcutaneous tumor growth. Proteomic studies showed that TLOC1 binds to DDX3X, which is essential for TLOC1-induced transformation and affected protein translation. SKIL induced invasion through upregulation of SLUG (SNAI2) expression. Together, these studies identify TLOC1 and SKIL as driver genes at 3q26 and more broadly suggest that cooperating genes may be co lified in other regions with somatic copy number gain. Significance: These studies identify TLOC1 and SKIL as driver genes in 3q26. These observations provide evidence that regions of somatic copy number gain may harbor cooperating genes of different but complementary functions. Cancer Discov 3(9) 1044–57. ©2013 AACR. This article is highlighted in the In This Issue feature, p. 953
Publisher: American Society for Clinical Investigation
Date: 05-2013
DOI: 10.1172/JCI66343
Publisher: Elsevier BV
Date: 03-2002
DOI: 10.1016/S1097-2765(02)00467-7
Abstract: Eukaryotic cells possess overlapping mechanisms to ensure that DNA replication is restricted to the S phase of the cell cycle. The levels of hOrc1p, the largest subunit of the human origin recognition complex, vary during the cell ision cycle. In rapidly proliferating cells, hOrc1p is expressed and targeted to chromatin as cells exit mitosis and prereplicative complexes are formed. Later, as cyclin A accumulates and cells enter S phase, hOrc1p is ubiquitinated on chromatin and then degraded. hOrc1p destruction occurs through the proteasome and is signaled in part by the SCF(Skp2) ubiquitin-ligase complex. Other hORC subunits are stable throughout the cell cycle. The regulation of hOrc1p may be an important mechanism in maintaining the ploidy in human cells.
No related grants have been discovered for So Young Kim.