Background: A previous study revealed that matrin-3 is an essential component in maintaining fibroblast growth factor 2 (FGF2)-mediated undifferentiation of neural stem cells (NSCs) using a proteomics approach. Malignant melanoma (MM) arises from melanocytes that originate from neural crest stem cells during development. Additionally, it has been reported that the expression of FGF2 is positively correlated with the progression of MM.

Objective: We expected that matrin-3, as a downstream component of FGF2, might be associated with the aggressiveness or differentiation of MM.

Methods: Matrin-3 expression was measured in human melanoma patient tissues and human MM cell lines. We analyzed the effect of matrin-3 siRNA on the proliferation of human MM cell lines and focused on cell cycle progression and apoptosis. We carried out in vivo xenograft tumor experiments by implanting A375 cells transfected with matrin-3 shRNA.

Results: Matrin-3 was highly expressed in MM, and matrin-3 knockdown inhibited the proliferation of melanoma cellsin vivo and in vitro. Furthermore, we found that matrin-3 knockdown led to an accumulation of cells in the G1 phase and an increase in apoptotic cell number.

Conclusion: Our results suggest that matrin-3 could be a new therapeutic target for the treatment of MM.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jdermsci.2020.08.013DOI Listing

Publication Analysis

Top Keywords

matrin-3
10
cell cycle
8
malignant melanoma
8
stem cells
8
human cell
8
cell lines
8
matrin-3 knockdown
8
cell
5
matrin-3 plays
4
plays role
4

Similar Publications

The nuclear matrix, a proteinaceous gel composed of proteins and RNA, is an important nuclear structure that supports chromatin architecture, but its role in human pluripotent stem cells (hPSCs) has not been described. Here we show that by disrupting heterogeneous nuclear ribonucleoprotein U (HNRNPU) or the nuclear matrix protein, Matrin-3, primed hPSCs adopted features of the naive pluripotent state, including morphology and upregulation of naive-specific marker genes. We demonstrate that HNRNPU depletion leads to increased chromatin accessibility, reduced DNA contacts and increased nuclear size.

View Article and Find Full Text PDF

Liver matrin-3 protects mice against hepatic steatosis and stress response via constitutive androstane receptor.

Mol Metab

August 2024

Department of Biochemistry, University of Nebraska - Lincoln, Beadle Center, 1901 Vine St, Lincoln, NE 68588, USA; Nebraska Center for Integrated Biomolecular Communication (NCIBC), University of Nebraska - Lincoln, Lincoln, NE 68588, USA; Nebraska Center for the Prevention of Obesity Diseases through Dietary Molecules, University of Nebraska - Lincoln, USA. Electronic address:

Article Synopsis
  • Researchers are studying a liver disease called MASLD, which is getting more common because many people are becoming overweight, and they want to find better treatments.
  • They looked at a protein called Matrin-3 that helps control how genes work in the liver and its role in preventing fat buildup and stress responses.
  • When Matrin-3 was removed from certain mice, it made their livers worse when they ate a high-fat diet, showing that Matrin-3 is important for keeping liver health by helping a special receptor called CAR function properly.
View Article and Find Full Text PDF

Matrin-3 (MATR3) was initially discovered as a component of the nuclear matrix about thirty years ago. Since then, accumulating studies have provided evidence that MATR3 not only plays a structural role in the nucleus, but that it is also an active protein involved in regulating gene expression at multiple levels, including chromatin organization, DNA transcription, RNA metabolism, and protein translation in the nucleus and cytoplasm. Furthermore, MATR3 may play a critical role in various cellular processes, including DNA damage response, cell proliferation, differentiation, and survival.

View Article and Find Full Text PDF

The role of Matrin-3 in physiology and its dysregulation in disease.

Biochem Soc Trans

June 2024

Department of Chemistry, Washington University, St. Louis, MO 63130, U.S.A.

The dysfunction of many RNA-binding proteins (RBPs) that are heavily disordered, including TDP-43 and FUS, are implicated in amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD). These proteins serve many important roles in the cell, and their capacity to form biomolecular condensates (BMCs) is key to their function, but also a vulnerability that can lead to misregulation and disease. Matrin-3 (MATR3) is an intrinsically disordered RBP implicated both genetically and pathologically in ALS/FTD, though it is relatively understudied as compared with TDP-43 and FUS.

View Article and Find Full Text PDF
Article Synopsis
  • MATR3 is an RNA-binding protein connected to neurodegenerative and neurodevelopmental diseases, but its role in cryptic splicing is not well understood.
  • Loss of MATR3 leads to the inclusion of cryptic exons in various transcripts, significantly affecting gene function.
  • Disease-associated variants, like S85C and M548T, impact MATR3 by reducing its solubility and altering its ability to bind RNA and regulate cryptic splicing.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!