Related Experiment Video
Updated: Dec 23, 2025

Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue
Published on: October 12, 2013
LINC00312/YBX1 Axis Regulates Myofibroblast Activities in Oral Submucous Fibrosis
Chuan-Hang Yu1,2,3, Chih-Yuan Fang4,5, Cheng-Chia Yu1,2,3
1School of Dentistry, Chung Shan Medical University, Taichung 40201, Taiwan.
Abstract:
Oral submucous fibrosis (OSF) has been recognized as a precancerous disorder in the oral cavity. Great effort has been made to inhibit the malignant progression of OSF over the past decades, but the cure of this fibrosis disease has not been discovered. In the present study, we found that a long noncoding RNA, LINC00312, was upregulated in OSF tissues, and positively associated with several fibrosis factors, such as α-SMA, type I collagen, and fibronectin. As such, we sought to investigate the role of LINC00312 in OSF progression and identify its interacting factor that mediated oral fibrogenesis. Our results showed that the inhibition of LINC00312 downregulated the myofibroblast activities, including collagen gel contractility, transwell migration, and wound healing, as well as the gene expression of myofibroblast markers. We verified that YBX1 was a downstream factor of LINC00312 and revealed that the downregulation of YBX1 repressed the gene expression of α-SMA and p-Smad2 along with the reduced myofibroblast phenotypes. Most importantly, we demonstrated that the LINC00312-induced myofibroblast activities were reverted by the knockdown of YBX1, suggesting that the LINC00312-mediated myofibroblast transdifferentiation was through YBX1. Collectively, our findings revealed that the LINC00312/ YBX1 axis may serve as a target for the development of therapies against OSF.
Insights
Researchers identified LINC00312 as a key factor in oral submucous fibrosis (OSF) progression. Targeting the LINC00312/YBX1 pathway shows promise for developing new therapies for this precancerous oral condition.
Area of Science:
- Oral pathology
- Molecular biology
- Oncology
Background:
- Oral submucous fibrosis (OSF) is a precancerous condition with no known cure.
- Malignant progression of OSF remains a significant clinical challenge.
- Understanding the molecular mechanisms driving OSF is crucial for therapeutic development.
Purpose of the Study:
- To investigate the role of long noncoding RNA LINC00312 in oral submucous fibrosis (OSF) progression.
- To identify the downstream interacting factor of LINC00312 involved in oral fibrogenesis.
- To explore the therapeutic potential of targeting the LINC00312/YBX1 axis in OSF.
Main Methods:
- Analysis of LINC00312 expression in OSF tissues.
- Inhibition of LINC00312 and assessment of myofibroblast activity (e.g., collagen gel contractility, migration, wound healing).
- Verification of YBX1 as a downstream target and investigation of its role in myofibroblast gene expression (α-SMA, p-Smad2).
Main Results:
- LINC00312 was upregulated in OSF tissues and correlated with fibrosis markers.
- LINC00312 inhibition reduced myofibroblast activity and marker gene expression.
- YBX1 was identified as a downstream mediator; its downregulation repressed myofibroblast phenotypes.
- Knockdown of YBX1 reversed LINC00312-induced myofibroblast activities, confirming the LINC00312/YBX1 axis.
Conclusions:
- The LINC00312/YBX1 axis plays a critical role in mediating myofibroblast transdifferentiation in OSF.
- This axis represents a potential therapeutic target for treating oral submucous fibrosis.
- Further research into targeting LINC00312 and YBX1 could lead to novel OSF therapies.
More Related Videos
Related Concept Videos
Formation of Muscle Fibers from Myoblasts
Muscle progenitor cells (MPCs) are formed from the myotomes. MPCs express genes that encode the transcription factors Pax3 and Pax7. Along with Pax 3/7, other transcription...
Introduction to Fibroblasts
Cell Motility through Blebbing
Blebbing Through the Matrix
In multicellular...
TGF - β Signaling Pathway
Type IV Collagen of Basal Lamina
A type IV collagen molecule has six alpha chains which can...

