Asset Details
Do you wish to reserve the book?
OCT4B mediates hypoxia-induced cancer dissemination
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?
OCT4B mediates hypoxia-induced cancer dissemination
Do you wish to request the book?
OCT4B mediates hypoxia-induced cancer dissemination
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
OCT4B mediates hypoxia-induced cancer dissemination
2019
Overview
Hypoxia, the reduction of oxygen levels in cells or tissues, elicits a set of genes to adjust physiological and pathological demands during normal development and cancer progression. OCT4, a homeobox transcription factor, is essential for self-renewal of embryonic stem cells, but little is known about the role of OCT4 in non-germ-cell tumorigenesis. Here, we report that hypoxia stimulates a short isoform of OCT4, called OCT4B, via a HIF2α-dependent pathway to induce the epithelial–mesenchymal transition (EMT) and facilitate cancer dissemination. OCT4B overexpression decreased epithelial barrier properties, which led to an increase in cell migration and invasion in lung cancer cells. OCT4B knockdown attenuated HIF2α-induced EMT and inhibited cancer dissemination in cell-line and animal models. We observed that OCT4B bound the
SLUG
promoter and enhanced its expression, and
SLUG
silencing inhibited OCT4B-mediated EMT, accompanied with decreased cell migration and invasion. Correlation analysis revealed that
OCT4B
expression was significantly associated with the
SLUG
level in lung tumors. These results provide novel insights into OCT4B-mediated oncogenesis in cancer dissemination.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 38
/ 38/77
/ 38/89
/ 45
/ 45/29
/ 59/5
/ Animals
/ Basic Helix-Loop-Helix Transcription Factors - genetics
/ Basic Helix-Loop-Helix Transcription Factors - metabolism
/ Cancer
/ Cell Transformation, Neoplastic - genetics
/ Cell Transformation, Neoplastic - metabolism
/ Cell Transformation, Neoplastic - pathology
/ Epithelial-Mesenchymal Transition
/ Genes
/ Homeobox
/ Humans
/ Hypoxia
/ Male
/ Medicine
/ Mice
/ Neoplasm Proteins - genetics
/ Neoplasm Proteins - metabolism
/ Octamer Transcription Factor-3 - genetics
/ Octamer Transcription Factor-3 - metabolism
/ Oncology
/ Tumors
