YAP is an important regulatory factor for the apoptosis and EMT degree mediated by TGF-beta1.

On April 20, the international academic journal Scientific Reports reported online on the work of Song Jianguo of the Institute of Biochemistry and Cell Biology of the Shanghai Institute of Life Sciences of the Chinese Academy of Sciences, entitled YAP modulates TGF-beta-1-induced simultaneous apoptosis and EMT through upregation of the EGF receptor.
presents the latest research results on the interrelation and balance regulation of two distinct cell fates, with apoptosis caused by transformational growth factor (TGF)-beta1, and endocal-interstate transgeneration (EMT).
TGF-beta1 can induce apoptosis and EMT, two fundamentally different cell fates occur at the same time, that is, one part of the same type of cells occurs apoptosis, and the other part occurs EMT.
TGF-beta1 effect is essential for cell survival and embryonic development differentiation, as well as for the steady state of the organs of the formed tissue, but the effect of TGF-beta1 has not received the necessary attention in the relevant research, and there is a lack of basic understanding of the interrelation and balance regulation mechanisms of the two biological events that occur at the same time.
, the study of related issues is of great scientific significance.
YAP is a transcriptional auxiliary regulatory molecule that plays an important role in various physiological pathology processes.
that YAP is known to regulate cell survival.
stimulation of TGF-beta1 can cause both apoptosis and EMT in the mammary epithern cells.
Song Jianguo Research Group found that YAP plays a survival-enhancing role in mammary epithal cells, and its over-expression can block the apoptosis induced by TGF-beta1, while its knock-down can trigger spontaneous apoptosis of cells and significantly enhance the response of cells to the apoptosis induction effect of TGF-beta1.
results show that YAP is an important regulatory factor for the apoptosis and EMT degree mediated by TGF-beta1.
analysis shows that, on the one hand, YAP has no direct regulatory effect on TGF-beta1-induced EMT, and its knock-down does not inhibit TGF-beta1-induced EMT;
of the EGF's machinery show that the above effects of YAP-mediated are closely related to their increased expression and activity of EGF receptors, which also provides important experimental evidence for the role of EGF in the biological effects of TGF-beta1 mediated.
in short, the above study reveals that apoptosis and EMT, which occur at the same time as TGF-beta1 mediated, are mutually exclusive and interrelated processes that are regulated by certain factors and are therefore dynamically balanced.
the research work received financial support from the National Natural Science Foundation of China.
of research data is supported by the Public Technical Service Center of the Institute of Biotechnology and Cells.
.