Asset Details
Do you wish to reserve the book?
PPM1G‐mediated TBL1X mRNA splicing promotes cell migration in hepatocellular carcinoma
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?
PPM1G‐mediated TBL1X mRNA splicing promotes cell migration in hepatocellular carcinoma
Do you wish to request the book?
PPM1G‐mediated TBL1X mRNA splicing promotes cell migration in hepatocellular carcinoma
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
PPM1G‐mediated TBL1X mRNA splicing promotes cell migration in hepatocellular carcinoma
2025
Overview
The progression of hepatocellular carcinoma (HCC) is coincident with aberrant splicing of numerous tumor‐related genes. Identification of the tumor‐specific splice variants that facilitate HCC metastasis may provide a more comprehensive insight into the mechanisms of HCC metastasis. Through RNA sequencing and bioinformatic analyses, PPM1G was identified as a biomarker associated with HCC metastasis. Our data mapped a transcriptome‐wide landscape of alternative splicing events modulated by PPM1G in HCC. Notably, we characterized the exon six‐skipping transcript of TBL1X as an onco‐splice variant regulated by PPM1G. Experimental validation revealed the enrichment of TBL1X‐S in response to PPM1G overexpression. Moreover, mRNA stability analyses revealed that PPM1G prolonged the half‐life of the TBL1X‐S transcript. Both PPM1G and TBL1X‐S exhibited metastasis‐promoting phenotypes, with PPM1G‐driven metastasis in HCC being partially dependent on TBL1X‐S. Mechanistically, different TBL1X splice variants showed varying affinities for ZEB1, with TBL1X‐S significantly enhancing ZEB1 activation and repressing CDH1 transcription, potentially accelerating the epithelial‐mesenchymal transition (EMT) process. In conclusion, our study highlights the biological role of PPM1G and TBL1X‐S in tumor metastasis. The PPM1G/TBL1X‐S signaling axis presents a new view for investigating liver cancer metastasis mechanisms. In this study, we highlight the biological role of the PPM1G and TBL1X‐S variants in tumor metastasis. The PPM1G/TBL1X‐S signaling axis presents a new view for investigating liver cancer metastasis mechanisms.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
/ Animals
/ Cancer
/ Carcinoma, Hepatocellular - genetics
/ Carcinoma, Hepatocellular - metabolism
/ Carcinoma, Hepatocellular - pathology
/ Epithelial-Mesenchymal Transition - genetics
/ Gene Expression Regulation, Neoplastic
/ Genes
/ HCC
/ Hepatoma
/ Humans
/ Liver Neoplasms - metabolism
/ Male
/ Mice
/ Original
/ Plasmids
/ PPM1G
/ Protein Phosphatase 2C - genetics
/ Protein Phosphatase 2C - metabolism
/ Proteins
/ TBL1X
/ Tumors
