Asset Details
Do you wish to reserve the book?
BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activity
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activity
Do you wish to request the book?
BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activity
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activity
2020
Overview
Accumulating evidence indicates that hepatocellular carcinoma (HCC) tumorigenesis, recurrence, metastasis, and therapeutic resistance are strongly associated with liver cancer stem cells (CSCs), a rare subpopulation of highly tumorigenic cells with self-renewal capacity and differentiation potential. Previous studies identified B cell leukemia/lymphoma-11b (BCL11B) as a novel tumor suppressor with impressive capacity to restrain CSC traits. However, the implications of BCL11B in HCC remain unclear. In this study, we found that low BCL11B expression was an independent indicator for shorter overall survival (OS) and time to recurrence (TTR) for HCC patients with surgical resection. In vitro and in vivo experiments confirmed BCL11B as a tumor suppressor in HCC with inhibitory effects on proliferation, cell cycle progression, apoptosis, and mobility. Furthermore, BCL11B could suppress CSC traits, as evidenced by dramatically decreased tumor spheroid formation, self-renewal potential and drug resistance. A Cignal Finder Array and dual-luciferase activity reporter assays revealed that BCL11B could activate the transcription of P73 via an E2F1-dependent manner. Thus, we concluded that BCL11B is a strong suppressor of retaining CSC traits in HCC. Ectopic expression of BCL11B might be a promising strategy for anti-HCC treatment with the potential to cure HBV-related HCC regardless of P53 mutation status.
Publisher
Nature Publishing Group UK,Springer Nature B.V
Subject
/ 13/100
/ 13/106
/ 13/109
/ 13/2
/ 13/31
/ 13/51
/ 13/89
/ 13/95
/ 14/34
/ 42/100
/ 82/47
/ Animals
/ Antineoplastic Agents - pharmacology
/ Biomedical and Life Sciences
/ Carcinogenesis - drug effects
/ Carcinoma, Hepatocellular - pathology
/ Cell Movement - drug effects
/ Cell Proliferation - drug effects
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Lymphoma
/ Male
/ Mice
/ Neoplastic Stem Cells - drug effects
/ Repressor Proteins - pharmacology
/ Repressor Proteins - physiology
/ Tumor Protein p73 - physiology
/ Tumor Suppressor Protein p53 - genetics
/ Tumor Suppressor Protein p53 - physiology
/ Tumor Suppressor Proteins - pharmacology
