Asset Details
Do you wish to reserve the book?
COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells
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?
COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells
Do you wish to request the book?
COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells
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
COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells
2026
Overview
Epithelial‐to‐mesenchymal transition (EMT), driven by cues from the tumor microenvironment, is a critical initiator of metastatic progression. In breast cancer patients, elevated expression of cartilage oligomeric matrix protein (COMP) is associated with shorter survival and increased metastatic risk. Here, we investigated the role of COMP in regulating EMT in breast cancer. Breast cancer cells treated with recombinant COMP or engineered to overexpress COMP exhibited a marked decrease in the epithelial marker CDH1 and an increase in mesenchymal markers such as VIM and VCAN. Consistent with these in vitro findings, COMP‐expressing xenograft tumor tissues showed enhanced EMT characteristics. Functionally, COMP promoted increased migration and invasion of breast cancer cells in both autocrine and paracrine manners, dependent on its thrombospondin (TSP) and C‐terminal domains. We further identified protein TMEPAI (encoded by gene PMEPA1) as a functional COMP‐binding partner that mediates COMP‐induced EMT, primarily through interaction with the TSP domain of COMP. Mechanistically, COMP shifted transforming growth factor beta (TGFβ) signaling from canonical phosphorylated mothers against decapentaplegic homolog 2/3 (pSMAD2/3) activation toward pSMAD1/5, likely through its interaction with PMEPA1. This study suggests the COMP–PMEPA1 axis as a new driver of EMT in breast cancer models. This study reveals that cartilage oligomeric matrix protein (COMP) promotes epithelial‐to‐mesenchymal transition (EMT) in breast cancer. We identify PMEPA1 (protein TMEPAI) as a novel COMP‐binding partner that mediates EMT via binding to the TSP domains of COMP, establishing the COMP–PMEPA1 axis as a key EMT driver in breast cancer.
Publisher
John Wiley & Sons, Inc,Wiley
Subject
/ Animals
/ Breast Neoplasms - metabolism
/ Breast Neoplasms - pathology
/ Cartilage oligomeric matrix protein
/ Cartilage Oligomeric Matrix Protein - genetics
/ Cartilage Oligomeric Matrix Protein - metabolism
/ COMP
/ EMT
/ Epithelial-Mesenchymal Transition
/ Female
/ Humans
/ Hypoxia
/ Membrane Proteins - genetics
/ Membrane Proteins - metabolism
/ Mice
/ PMEPA1
/ Proteins
/ Transforming Growth Factor beta - metabolism
/ Tumors
