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KMID : 0391320000100020185
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Korean Journal of Biological Response Modifiers
2000 Volume.10 No. 2 p.185 ~ p.192
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Molecular Analysis of the Roles of TGF-β and TGF-β Signal Transduction Pathways in the Korean Stomach Cancer Carcinogenesis
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Lee Ki-Hyeong
Kim Seung-Taik
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Abstract
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Background: Identifying molecular markers to monitor the pathological processes of the disease so as to evaluate better patient prognosis and to elucidate molecular mechanism of stomach cancer initiation, progression and metastasis is very important to overcame this cancer. The TGF-β and TGF-β signaling pathways have been known to be involved in the carcinogenesis of many cancers. To evaluate the relationship of this factor to the development of stomach cancer, we analyzed the expression of the TGF-β type Ⅰ and type Ⅱ receptors and changes in TGF-β signaling pathways in stomach cancer.
Methods: Various stomach cell lines established in Korea were employed to study the responsiveness of cell growth to TGF-β and the role of the TGF-β type Ⅰ and type Ⅱ receptors which mediate the TGF-β actions. Expression of type Ⅱ receptors were elucidated with Northern blot analysis. Moreover, TGF-β signaling pathways in stomach cancer was analyzed through the examination of p53 and p21 expression in each cancer cell line with Western blot method.
Results: With the treatment of TGF-β, the growth was inhibited in case of SNU-16 and Kato cell line, whereas the growth was not inhibited in the SNU-1 and SNU-5 cell lines. The presence of TGF-β receptor type Ⅱ mRNA was evident in the SNU-16 cell line whose growth was suppressed with TGF-β. However, TGF-β receptor type Ⅱ gene was deleted completely or partially in the cell lines which did not respond to TGF-β. P53 proteins were expressed in the SNU-1 and SNU-16 cell lines examined regardless of their responsiveness to TGF-β. The increased expression of p21 was seen in the SNU-16 cell line under TGF-β, but P21 expression was not detected in the SNU-1 cell line.
Conclusion: Some stomach cancer cell line established in Korea did not respond to TGF-β, which was caused by abnormalities in the TGF-β receptor. One of the signaling pathways of the TGF-β was mediated by p21. The dependence of p53 in p21 expression could not be elucidated. In conclusion, loss of TGF-β responsiveness may be important in the growth of Korean stomach cancer.
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KEYWORD
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Stomach cancer, Transforming growth factor (TGF-β), TGF-β type Ⅰ and type Ⅱ receptors, signal pathway,
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