Abstract:
:Strikingly increased expression of notch-1 has been demonstrated in several human malignancies and pre-neoplastic lesions. However, the functional consequences of notch-1 overexpression in transformed cells remain unclear. We investigated whether endogenously expressed notch-1 controls cell fate determination in mouse erythroleukemia (MEL) cells during pharmacologically induced differentiation. We found that notch-1 expression is modulated during MEL cell differentiation. Premature downregulation of notch-1 during differentiation, by antisense S-oligonucleotides or by enforced expression of antisense notch-1 mRNA, causes MEL cells to abort the differentiation program and undergo apoptosis. Downregulation of notch-1 expression in the absence of differentiation inducer increases the likelihood of spontaneous apoptosis. We conclude that in MEL cells, endogenous notch-1 expression controls the apoptotic threshold during differentiation and growth. In these cells, notch-1 allows differentiation by preventing apoptosis of pre-committed cells. This novel function of notch-1 may play a role in regulating apoptosis susceptibility in notch-1 expressing tumor cells.
journal_name
J Cell Biochemjournal_title
Journal of cellular biochemistryauthors
Shelly LL,Fuchs C,Miele Ldoi
10.1002/(sici)1097-4644(19990501)73:2<164::aid-jcbsubject
Has Abstractpub_date
1999-05-01 00:00:00pages
164-75issue
2eissn
0730-2312issn
1097-4644pii
10.1002/(SICI)1097-4644(19990501)73:2<164::AID-JCBjournal_volume
73pub_type
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