Asset Details
Do you wish to reserve the book?
LIN28B fosters colon cancer migration, invasion and transformation through let-7-dependent and -independent mechanisms
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?
LIN28B fosters colon cancer migration, invasion and transformation through let-7-dependent and -independent mechanisms
Do you wish to request the book?
LIN28B fosters colon cancer migration, invasion and transformation through let-7-dependent and -independent mechanisms
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
LIN28B fosters colon cancer migration, invasion and transformation through let-7-dependent and -independent mechanisms
2011
Overview
Lin28b is an RNA-binding protein that inhibits biogenesis of
let-7
microRNAs.
LIN28B
is overexpressed in diverse cancers, yet a specific role in the molecular pathogenesis of colon cancer has to be elucidated. We have determined that human colon tumors exhibit decreased levels of mature
let-7
isoforms and increased expression of
LIN28B
. To determine
LIN28B
's mechanistic role in colon cancer, we expressed
LIN28B
in immortalized colonic epithelial cells and human colon cancer cell lines. We found that
LIN28B
promotes cell migration, invasion and transforms immortalized colonic epithelial cells. In addition, constitutive
LIN28B
expression increases expression of intestinal stem cell markers
LGR5
and
PROM1
in the presence of
let-7
restoration. This may occur as a result of Lin28b protein binding
LGR5
and
PROM1
mRNA, suggesting that a subset of
LIN28B
functions is independent of its ability to repress
let-7
. Our findings establish a new role for
LIN28B
in human colon cancer pathogenesis, and suggest
LIN28B
post-transcriptionally regulates
LGR5
and
PROM1
through a
let-7
-independent mechanism.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Biological and medical sciences
/ Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
/ Colonic Neoplasms - pathology
/ DNA-Binding Proteins - physiology
/ Fundamental and applied biological sciences. Psychology
/ Gastroenterology. Liver. Pancreas. Abdomen
/ Humans
/ Isoforms
/ Medicine
/ miRNA
/ Molecular and cellular biology
/ mRNA
/ Oncology
/ Proteins
/ RNA
/ Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
/ Tumors
