Related Experiment Video

Updated: May 30, 2026

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
11:29

miRNA Expression Analyses in Prostate Cancer Clinical Tissues

Published on: September 8, 2015

Maspin expression is regulated by the non-canonical NF-κB subunit in androgen-insensitive prostate cancer cell lines

Feng Guo1, Suya Kang, Peng Zhou

  • 1Central Lab, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. guofeng27@suda.edu.cn

Molecular Immunology
|August 23, 2011
PubMed

Insights

In advanced prostate cancer, RelB protein actively suppresses the tumor suppressor Maspin. Targeting RelB could help re-establish Maspin expression for treating metastatic disease.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Dysregulated Maspin expression and constitutive NF-κB activation are hallmarks of prostate cancer.
  • RelB, a component of the alternative NF-κB pathway, influences prostate carcinogenesis.
  • Both classical and alternative NF-κB pathways are constitutively active in androgen-insensitive prostate cancer cells.

Purpose of the Study:

  • To investigate the relationship between Maspin and RelB expression in prostate cancer.
  • To elucidate the role of RelB in regulating Maspin expression.
  • To explore the therapeutic potential of targeting RelB in advanced prostate cancer.

Main Methods:

  • Analysis of Maspin and RelB expression correlation in prostate cancer tissues.
  • Investigation of TNF-α signaling effects on RelB and Maspin.
  • Studies using proteasome inhibitors to modulate Maspin and RelB levels.
  • Gene depletion and enforced expression experiments to determine RelB's function.
  • Cellular assays in androgen-insensitive human prostate cancer cells.

Main Results:

  • A negative correlation between Maspin and RelB expression was observed in late-stage prostate cancer.
  • TNF-α signaling induced RelB nuclear accumulation and reduced Maspin expression.
  • Proteasome inhibitor-induced Maspin expression was linked to decreased RelB levels.
  • RelB depletion, but not RelA depletion, induced Maspin expression.
  • RelB deficiency blocked proteasome inhibitor-induced Maspin expression.
  • Enforced RelB expression inhibited Maspin expression in prostate cancer cells.

Conclusions:

  • RelB is a key regulator of both endogenous and proteasome inhibitor-induced Maspin expression.
  • RelB acts as a suppressor of Maspin in prostate cancer.
  • Targeting RelB may offer a therapeutic strategy for advanced, metastatic prostate cancer by restoring Maspin's tumor-suppressive function.

More Related Videos

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR (qPCR)08:30

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR (qPCR)

Published on: May 16, 2012

Murine Prostate Micro-dissection and Surgical Castration08:49

Murine Prostate Micro-dissection and Surgical Castration

Published on: May 11, 2016

Related Concept Videos

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...
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...
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...
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...
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...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...