MbrlCatalogueTitleDetail

Do you wish to reserve the book?
PVT1‐derived miR‐1207‐5p promotes breast cancer cell growth by targeting STAT6
PVT1‐derived miR‐1207‐5p promotes breast cancer cell growth by targeting STAT6
Hey, we have placed the reservation for you!
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.
You are currently in the queue to collect this book. You will be notified once it is your turn to collect the book.
Oops! Something went wrong.
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?
PVT1‐derived miR‐1207‐5p promotes breast cancer cell growth by targeting STAT6
Oops! Something went wrong.
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Title added to your shelf!
Title added to your shelf!
View what I already have on My Shelf.
Oops! Something went wrong.
Oops! Something went wrong.
While trying to add the title to your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
PVT1‐derived miR‐1207‐5p promotes breast cancer cell growth by targeting STAT6
PVT1‐derived miR‐1207‐5p promotes breast cancer cell growth by targeting STAT6

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
How would you like to get it?
We have requested the book for you! Sorry the robot delivery is not available at the moment
We have requested the book for you!
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.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
PVT1‐derived miR‐1207‐5p promotes breast cancer cell growth by targeting STAT6
PVT1‐derived miR‐1207‐5p promotes breast cancer cell growth by targeting STAT6
Journal Article

PVT1‐derived miR‐1207‐5p promotes breast cancer cell growth by targeting STAT6

2017
Request Book From Autostore and Choose the Collection Method
Overview
Accumulating evidence indicates that ectopic expression of non‐coding RNAs are responsible for breast cancer progression. Increased non‐coding RNA PVT1, the host gene of microRNA‐1207‐5p (miR‐1207‐5p), has been associated with breast cancer proliferation. However, how PVT1 functions in breast cancer is still not clear. In this study, we show a PVT1‐derived microRNA, miR‐1207‐5p, that promotes the proliferation of breast cancer cells by directly regulating STAT6. We first confirm the positive correlated expression pattern between PVT1 and miR‐1207‐5p by observing consistent induced expression by estrogen, and overexpression in breast cancer cell lines and breast cancer patient specimens. Moreover, silence of PVT1 also decreased miR‐1207‐5p expression. Furthermore, increased miR‐1207‐5p expression promoted, while decreased miR‐1207‐5p expression suppressed, cell proliferation, colony formation, and cell cycle progression in breast cancer cell lines. Mechanistically, a novel target of miR‐1207‐5p, STAT6, was identified by a luciferase reporter assay. Overexpression of miR‐1207‐5p decreased the levels of STAT6, which activated CDKN1A and CDKN1B to regulate the cell cycle. We also confirmed the reverse correlation of miR‐1207‐5p and STAT6 expression levels in breast cancer samples. Therefore, our findings reveal that PVT1‐derived miR‐1207‐5p promotes the proliferation of breast cancer cells by targeting STAT6, which in turn controls CDKN1A and CDKN1B expression. These findings suggest miR‐1207‐5p might be a potential target for breast cancer therapy. our findings demonstrate that PVT1‐derived miR‐1207‐5p promotes the proliferation of breast cancer cells by targeting STAT6, which in turn controls CDKN1A and CDKN1B expression. These findings suggest miR‐1207‐5p might be a potential target for breast cancer therapy.