mysteries of tgf-β paradox in benign and malignant cells
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ID: 212748
2014
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Abstract
TGF-β regulates a wide range of biological functions including embryonic development, wound healing, organogenesis, immune modulation, and cancer progression. Interestingly, TGF-β is known to inhibit cell growth in benign cells but promote progression in cancer cells, a phenomenon known as TGF-β paradox. To date, the mechanism of this paradox still remains as a scientific mystery. In this review, we present our experience, alone with the literature, in an attempt to offer answers to this mystery. First, we observed that, upon TGF-β engagement, there is a differential activation of Erk between benign and cancer cells. Since activated Erk is a major mediator in tumor progression and metastasis, a differentially activated Erk represents the answer to this mystery. Second, we identified a key player, PP2A-B56α, which is differentially recruited by the activated type I TGF-β receptor (TBRI) in benign and tumor cells, resulting in differential Erk activation. Finally, TGF-β stimulation leads to a suppressed TBRs in tumor cells but not in benign cells. This differentially suppressed TBRs triggers differential recruitment of PP2A-B56α and, thus, differential activation of Erk. The above three events offer the explanation to the mysteries
| Reference Key |
elee2014frontiersmysteries
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|---|---|
| Authors | ;Chung eLee;Chung eLee;Chung eLee |
| Journal | international journal of heat and technology |
| Year | 2014 |
| DOI |
10.3389/fonc.2014.00094
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| URL | |
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