Related Experiment Video

Updated: Aug 19, 2026

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
09:58

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis

Published on: June 27, 2020

Myxoid liposarcoma FUS-DDIT3 fusion oncogene induces C/EBP beta-mediated interleukin 6 expression

Melker Göransson1, Erik Elias, Anders Ståhlberg

  • 1Lundberg Laboratory for Cancer Research (LLCR), Department of Pathology, Goteborg University, Gothenburg, Sweden. melker.goransson@llcr.med.gu.se

International Journal of Cancer
|February 3, 2005
PubMed

Insights

The FUS-DDIT3 oncogene upregulates interleukin 6 (IL6) in liposarcoma cells, dependent on C/EBP beta. This study reveals new insights into FUS-DDIT3

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Expression Analysis

Background:

  • The FUS-DDIT3 oncogene, a fusion of FUS and DDIT3, drives myxoid/round cell liposarcoma.
  • Understanding downstream targets and transforming effects of FUS-DDIT3 is crucial for liposarcoma research.

Purpose of the Study:

  • To investigate the downstream targets of DDIT3.
  • To explore the transforming effects of the FUS-DDIT3 fusion protein.
  • To analyze gene expression profiles in response to DDIT3 and FUS-DDIT3 expression.

Main Methods:

  • Gene expression profiling using microarray analysis.
  • Stable transfection of human fibrosarcoma cell lines with DDIT3-GFP and FUS-DDIT3-GFP constructs.
  • Quantitative analysis of mRNA and protein expression.
  • siRNA-mediated knockdown of CEBPB transcripts.
  • Chromatin immunoprecipitation (ChIP) assays.
  • Real-time PCR for gene expression analysis.

Main Results:

  • Interleukin 6 (IL6) is upregulated in fibrosarcoma cell lines expressing DDIT3 and FUS-DDIT3, as well as in myxoid liposarcoma cell lines.
  • IL6 upregulation is dependent on C/EBP beta, with FUS-DDIT3 directly interacting with the IL6 promoter via C/EBP beta.
  • DDIT3 and FUS-DDIT3 exhibit opposing transcriptional regulation of IL8.
  • FUS-DDIT3 may influence synergistic activation of promoters regulated by C/EBP beta and NFkappaB.

Conclusions:

  • FUS-DDIT3 oncogene drives IL6 expression in a C/EBP beta-dependent manner.
  • The study elucidates a novel regulatory mechanism involving FUS-DDIT3, C/EBP beta, and IL6 in liposarcoma pathogenesis.
  • Differential regulation of acute phase genes like IL8 by DDIT3 and FUS-DDIT3 suggests distinct functional roles.

More Related Videos

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells10:21

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...