RT Journal Article
SR Electronic
T1 Sensitization against Anticancer Drugs by Transfection with UBE2I Variant Gene into ras-NIH3H3 Mouse Fibroblasts
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 3227
OP 3233
VO 27
IS 5A
A1 SHIRATORI, TOORU
A1 SHIMADA, HIDEAKI
A1 KAGAYA, AKIKO
A1 KUBOSHIMA, MARI
A1 NABEYA, YOSHIHIRO
A1 MACHIDA, TOSHIO
A1 GOTO, KEN-ICHIRO
A1 TAKIGUCHI, MASAKI
A1 OCHIAI, TAKENORI
A1 HIWASA, TAKAKI
YR 2007
UL http://ar.iiarjournals.org/content/27/5A/3227.abstract
AB We previously performed SEREX (serological identification of antigens by recombinant expression cloning) using the sera of patients with esophageal squamous cell carcinoma (SCC), and isolated a variant clone (AK093616) of ubiquitin-conjugating enzyme E2I (UBE2I). This clone was tentatively designated as UBE2I-v5 and analyzed for biological function by transient transfection of the cDNA into activated Ha-ras-transformed NIH3T3 (ras-NIH) mouse fibroblasts. Chemosensitivity to 92 cytotoxic drugs was compared between UBE2I-v5-transfected cells and the parental ras-NIH cells. The UBE2I-v5-transfected cells were more sensitive than the parental cells to anticancer drugs such as vincristine (VCR), mitoxantrone (MIT) and etoposide (VP-16). The regression analysis of the total chemosensitivity pattern of UBE2I-v5-transfected cells revealed that the function of UBE2I-v5 was positively related to RPA2 (replication protein A2), Rho-GDI (Rho guanine nucleotide dissociation inhibitor α), FUS (putative tumor suppressor) and TKT (transketolase) but negatively related to Per-1 (period-1), Ran (nuclear Ras-related protein), PTEN (phosphatase and tensin homolog), C/EBPα (CCAAT/enhancer binding protein α) and the tumor suppressor p53. Thus, it is possible that UBE2I-v5 plays a role in carcinogenesis by suppressing the function of C/EBPα and/or p53 via RPA2-like activity. Copyright© 2007 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved