Human Rad17 is phosphorylated upon DNA damage and also overexpressed in primary non-small cell lung cancer tissues

Citation
X. Wang et al., Human Rad17 is phosphorylated upon DNA damage and also overexpressed in primary non-small cell lung cancer tissues, CANCER RES, 61(20), 2001, pp. 7417-7421
Citations number
28
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
CANCER RESEARCH
ISSN journal
00085472 → ACNP
Volume
61
Issue
20
Year of publication
2001
Pages
7417 - 7421
Database
ISI
SICI code
0008-5472(20011015)61:20<7417:HRIPUD>2.0.ZU;2-T
Abstract
The spRAD17 gene is an essential component of the DNA damage and replicatio n checkpoints, in the fission yeast Schizosaccharomyces pombe. Cloning of t he human homologue of spRAD17, hRAD17, indicate that exhibits structural si milarity with the replication accessory protein family, which include subun its of the Replication factor C complex. We have analyzed the phosphorylati on status of hRad17 in response to DNA damaging agents. Our results showed that phosphorylation of hRad17 occurred immediately after UV and ionizing r adiation treatment and reached peak level at similar to3 h, suggesting that hRad17 may be a component of the DNA damage checkpoint. When primary tumor samples were analyzed, we observed that the majority (74%) of non-small ce ll lung carcinoma samples exhibited a significantly higher level of hRad17 expression compared with matched normal tissue controls. In contrast, hRad1 7 protein levels in a panel of primary colon carcinoma samples did not show an elevated level of expression compared with normal colon tissues. This o bservation suggests that the function of the hRAD17 gene may be involved in lung cancer development and may serve as a potential tumor marker.