Asset Details
Do you wish to reserve the book?
Oncogenic splicing abnormalities induced by DEAD‐Box Helicase 56 amplification in colorectal cancer
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?
Oncogenic splicing abnormalities induced by DEAD‐Box Helicase 56 amplification in colorectal cancer
Do you wish to request the book?
Oncogenic splicing abnormalities induced by DEAD‐Box Helicase 56 amplification in colorectal cancer
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
Oncogenic splicing abnormalities induced by DEAD‐Box Helicase 56 amplification in colorectal cancer
2019
Overview
Alternative splicing, regulated by DEAD‐Box Helicase (DDX) families, plays an important role in cancer. However, the relationship between the DDX family and cancer has not been fully elucidated. In the present study, we identified a candidate oncogene DDX56 on Ch.7p by a bioinformatics approach using The Cancer Genome Atlas (TCGA) dataset of colorectal cancer (CRC). DDX56 expression was measured by RT‐qPCR and immunochemical staining in 108 CRC patients. Clinicopathological and survival analyses were carried out using three CRC datasets. Biological roles of DDX56 were explored by gene set enrichment analysis (GSEA), and cell proliferation in vitro and in vivo, cell cycle assays, and using DDX56‐knockdown or overexpressed CRC cells. RNA sequencing was carried out to elucidate the effect of DDX56 on mRNA splicing. We found that DDX56 expression was positively correlated with the amplification of DDX56 and was upregulated in CRC cells. High DDX56 expression was associated with lymphatic invasion and distant metastasis and was an independent poor prognostic factor. In vitro analysis, in vivo analysis and GSEA showed that DDX56 promoted proliferation ability through regulating the cell cycle. DDX56 knockdown reduced intron retention and tumor suppressor WEE1 expression, which functions as a G2‐M DNA damage checkpoint. We have identified DDX56 as a novel oncogene and prognostic biomarker of CRC that promotes alternative splicing of WEE1. We identified DDX56 as a novel oncogene on chromosome 7p and a prognostic biomarker of colorectal cancer (CRC). DDX56 can induce oncogenic splicing abnormalities of the G2‐M cell cycle checkpoint gene WEE1 which contributes to the inhibition of proliferation and cell cycle progression.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
/ Animals
/ Cancer
/ Cell Cycle Proteins - genetics
/ Chromosomes, Human, Pair 7 - genetics
/ Colorectal Neoplasms - genetics
/ Colorectal Neoplasms - metabolism
/ Colorectal Neoplasms - pathology
/ Datasets
/ DEAD-box RNA Helicases - genetics
/ DEAD-box RNA Helicases - metabolism
/ DEAD‐Box Helicase 56 (DDX56)
/ DNA
/ Female
/ Gene Expression Regulation, Neoplastic
/ Gene set enrichment analysis
/ Genomes
/ Grants
/ Humans
/ Kinases
/ Male
/ Mice
/ mRNA
/ oncogene
/ Original
/ Protein-Tyrosine Kinases - genetics
/ Tumors
