Related Experiment Video
Updated: Mar 20, 2026
Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
Published on: November 28, 2015
Jumonji AT-rich interactive domain 1B overexpression is associated with the development and progression of glioma
Liping Fang1, Jiuhan Zhao2, Dan Wang3
1Department of Oncology 5, The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116023, P.R. China.
Abstract:
Previous studies have suggested that jumonji AT-rich interactive domain 1B (JARID1B) plays an important role in the genesis of some types of cancer, and it is therefore considered to be an important drug target protein. Although the expression of JARID1B has been researched in some types of cancer, little is known about JARID1B expression in glioma and its function in the tumorigenesis of gliomas. In the present study, we examined the expression of JARID1B in glioma. In addition, RT-PCR, western blot analysis and immunohistochemical analysis were performed using glioma tissue samples and the results revealed that JARID1B expression increased according to the histological grade of glioma. However, in the normal brain tissue samples JARID1B expression was barely detected. Kaplan‑Meier analysis revealed that higher JARID1B expression in patients with glioma was associated with a poorer prognosis. The overexpression of JARID1B stimulated the proliferation and migration of glioma cells as well as sphere formation, whereas suppressing the expression of JARID1B produced opposite effects. The overexpression of JARID1B increased the tumorigenicity of glioma cells in vivo in a nude mouse xenograft model of glioma. Moreover, the activation of phosphorylated (p-)Smad2 contributes to JARID1B-induced oncogenic activities. These findings suggest that JARID1B is involved in the pathogenesis of glioma, and that the downregulation of JARID1B in glioma cells may be a therapeutic target for the treatment of patients with glioma.
Insights
Jumonji AT-rich interactive domain 1B (JARID1B) is upregulated in glioma and linked to poorer patient prognosis. Inhibiting JARID1B may offer a new therapeutic strategy for glioma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Neuroscience
Background:
- Jumonji AT-rich interactive domain 1B (JARID1B) is implicated in various cancers, making it a potential drug target.
- JARID1B's role in glioma development and its expression patterns remain largely uncharacterized.
Purpose of the Study:
- To investigate the expression of JARID1B in glioma tissues.
- To elucidate the functional role of JARID1B in glioma tumorigenesis and its association with patient prognosis.
Main Methods:
- RT-PCR, Western blot, and immunohistochemical analysis were used to assess JARID1B expression in glioma samples.
- In vitro cell proliferation, migration, and sphere formation assays were conducted.
- In vivo tumorigenicity was evaluated using a nude mouse xenograft model.
- Phosphorylated Smad2 activation was analyzed.
Main Results:
- JARID1B expression significantly increases with glioma histological grade and is minimally detected in normal brain tissue.
- Higher JARID1B expression correlates with poorer patient prognosis.
- JARID1B overexpression enhances glioma cell proliferation, migration, sphere formation, and in vivo tumorigenicity.
- JARID1B-induced oncogenic activities involve the activation of phosphorylated Smad2.
Conclusions:
- JARID1B is involved in glioma pathogenesis and progression.
- JARID1B represents a potential therapeutic target for glioma treatment, with downregulation showing promise.
More Related Videos
09:40Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
05:45Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections
Published on: July 31, 2017
Related Concept Videos
02:07Tumor Progression
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
02:07Tumor Progression
01:20The Retinoblastoma Gene
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
01:20The Retinoblastoma Gene
01:22PI3K/mTOR/AKT Signaling Pathway
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...