Abstract:
:DPC4/SMAD4 is a candidate tumor suppressor gene with a strikingly high frequency of gene alterations in pancreatic cancer that suggests a discrete role for DPC4 in these tumors. DPC4 tumor-suppressive function has been implicated to mediate the transforming growth factor-beta (TGFbeta)-suppressive pathway; however, in a DPC4-null pancreatic cancer cell line, TGFbeta growth-inhibitory and transcriptional responses were found to be DPC4-independent. This was observed within native cells having a natural homozygous deletion and in clones engineered for stable expression of wild-type DPC4 integrated into the genome. This observation contrasted with the absolute DPC4 dependence of TGFbeta responses in a breast cancer cell line studied in parallel. This growth-inhibitory response to TGFbeta in DPC4-null cells relied on an intact ras effector pathway. These data further suggest a major categorization of TGFbeta responses into DPC4-dependent and -independent signaling pathways and specifically suggest that disruption of the TGFbeta-independent signal might be a basis of selection for the emergence of DPC4 alterations during tumorigenesis in the pancreas and other sites.
journal_name
Mol Carcinogjournal_title
Molecular carcinogenesisauthors
Dai JL,Schutte M,Bansal RK,Wilentz RE,Sugar AY,Kern SEdoi
10.1002/(sici)1098-2744(199909)26:1<37::aid-mc5>3.subject
Has Abstractpub_date
1999-09-01 00:00:00pages
37-43issue
1eissn
0899-1987issn
1098-2744pii
10.1002/(SICI)1098-2744(199909)26:1<37::AID-MC5>3.journal_volume
26pub_type
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