Please use this identifier to cite or link to this item:
https://scholarbank.nus.edu.sg/handle/10635/30274
Title: | Role of protein misfolding pathway in HBX-induced hepatocellular carcinoma (HCC) | Authors: | TAN SU YIN | Keywords: | HBX, N-CoR, HCC, protein misfolding, ER stress, Autophagy | Issue Date: | 17-Aug-2011 | Citation: | TAN SU YIN (2011-08-17). Role of protein misfolding pathway in HBX-induced hepatocellular carcinoma (HCC). ScholarBank@NUS Repository. | Abstract: | Transcriptional control imparted by nuclear receptor co-repressor (N-CoR) plays an important role in the growth suppressive function of several tumour suppressor proteins. Abrogation of this transcriptional control due to a misfolded conformation dependent loss (MCDL) of N-CoR has been implicated in acute promyelocytic leukemia (APL). It was hypothesized that an APL like MCDL of N- CoR might be involved in other malignancy. Indeed, the initial screening of N-CoR status in various liver cancer (HCC) cell lines revealed an APL like MCDL of N-CoR protein. The N-CoR protein presented in these HCC cells was misfolded and was linked to the amplification of endoplasmic reticulum (ER) stress and cytoprotective unfolded protein response (UPR). siRNA-induced N-CoR ablation led to selective reduction of intracellular ATP level and significantly compromised the growth of HCC cells, suggesting an important role of energy, possibly derived from N-CoR catabolism, in HCC cell growth. These findings identify an important role of autophagy-induced recycling of misfolded N-CoR protein in the selective activation of autonomous survival and growth in HCC cells. | URI: | http://scholarbank.nus.edu.sg/handle/10635/30274 |
Appears in Collections: | Master's Theses (Open) |
Show full item record
Files in This Item:
File | Description | Size | Format | Access Settings | Version | |
---|---|---|---|---|---|---|
TanSuYinThesis2011.pdf | 3.71 MB | Adobe PDF | OPEN | None | View/Download |
Google ScholarTM
Check
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.