Related Experiment Video

Updated: Jun 9, 2026

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

Vitamin D3 upregulated protein 1 suppresses TNF-α-induced NF-κB activation in hepatocarcinogenesis

Hyo-Jung Kwon1, Young-Suk Won, Hyun-Woo Suh

  • 1Bio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk, South Korea.

Journal of Immunology (Baltimore, Md. : 1950)
|September 10, 2010
PubMed

Insights

Vitamin D(3) upregulated protein 1 (VDUP1) suppresses liver cancer by inhibiting TNF-α-induced NF-κB activation. VDUP1 deficiency increases susceptibility to liver carcinogenesis and promotes tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Hepatology

Background:

  • Vitamin D(3) upregulated protein 1 (VDUP1) is a potential tumor suppressor with reduced expression in tumors.
  • Hepatic carcinogenesis involves complex molecular pathways affecting cell growth and regulation.

Purpose of the Study:

  • To investigate the role of VDUP1 in hepatocarcinogenesis.
  • To elucidate the molecular mechanisms by which VDUP1 regulates liver cancer development.

Main Methods:

  • Comparative analysis of VDUP1 expression in human liver cancer tissues and normal tissues.
  • Assessment of hepatocarcinogenesis in VDUP1-deficient mice compared to wild-type mice.
  • Examination of cell cycle regulatory proteins, TNF-α release, and NF-κB activation in response to VDUP1 levels and hepatomitogens.

Main Results:

  • VDUP1 expression is suppressed during human hepatic carcinogenesis.
  • VDUP1-deficient mice exhibit increased susceptibility to chemically induced liver cancer, with more aggressive tumor proliferation.
  • VDUP1 deficiency enhances TNF-α release and NF-κB activation, while VDUP1 overexpression suppresses TNF-α-activated NF-κB via HDAC1/HDAC3 association.

Conclusions:

  • VDUP1 acts as a negative regulator of hepatocarcinogenesis.
  • VDUP1 suppresses liver cancer progression by inhibiting TNF-α-induced NF-κB signaling pathway.

More Related Videos

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia09:52

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

Published on: December 4, 2018

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Co-activators and Co-repressors02:04

Co-activators and Co-repressors

Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...