Related Experiment Video

Updated: Aug 17, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

The role of c-Jun in the AP-1 activation induced by naturally occurring isothiocyanates

J Li1, S Yao, Y Zhang

  • 1Department of Chemoprevention, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|July 2, 2005
PubMed

Insights

Certain isothiocyanates (ITCs) may promote bladder cancer by activating c-Jun. This study identifies c-Jun activation as a key mechanism in isothiocyanate-induced bladder carcinogenesis, offering insights into cancer promotion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Carcinogenesis

Background:

  • Isothiocyanates (ITCs) show mixed effects on cancer, with some inhibiting and others potentially promoting carcinogenesis.
  • The molecular mechanisms underlying ITC-induced carcinogenesis are not well understood.

Purpose of the Study:

  • To investigate the molecular basis of how certain ITCs induce or promote bladder cancer.
  • To identify the specific molecular pathways involved in ITC-induced bladder carcinogenesis.

Main Methods:

  • Utilized human bladder cancer cell lines (UM-UC-3) and rat bladder cancer cell lines.
  • Assessed the transactivation and DNA binding of activator protein 1 (AP-1) in response to ITCs.
  • Examined the expression levels of Fos and Jun family members, focusing on c-Jun and Fra-2.
  • Investigated the role of c-Jun N-terminal kinase (JNK) in ITC-induced c-Jun activation.

Main Results:

  • Allyl ITC, benzyl ITC, and phenethyl ITC increased AP-1 transactivation and DNA binding in human bladder cancer cells.
  • c-Jun and Fra-2 levels were elevated by ITCs, with c-Jun identified as the predominant component in the AP-1 DNA binding complex.
  • ITC-induced c-Jun was observed in various human and rat bladder cancer cell lines and their metabolites.
  • ITC exposure activated c-Jun through transcriptional activation and protein phosphorylation, involving JNK activation.

Conclusions:

  • c-Jun activation plays a significant role in the bladder carcinogenesis induced by certain ITCs.
  • The findings suggest that c-Jun activation is a key molecular mechanism underlying ITC-induced bladder cancer promotion.

More Related Videos

A Pre-Clinical Model of Synovitis Using Ex vivo Human Synovial Tissue with Preserved Function and Architecture08:32

A Pre-Clinical Model of Synovitis Using Ex vivo Human Synovial Tissue with Preserved Function and Architecture

Published on: March 20, 2026

Related Concept Videos

Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
Allosteric Proteins-ATCase01:19

Allosteric Proteins-ATCase

Binding sites linkages can regulate a protein's function.  For example, enzyme activity is often regulated through a feedback mechanism where the end product of the biochemical process serves as an inhibitor.
Aspartate transcarbamoylase (ATCase) is a cytosolic enzyme that catalyzes the condensation of L-aspartate and carbamoyl phosphate to  N-carbamoyl-L-aspartate. This reaction is the first step in pyrimidine biosynthesis. UTP and CTP, the end products of the pyrimidine synthesis pathway,...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...