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Related Concept Videos

The Proteasome02:18

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important amongst these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. A series of enzymes carry out the ubiquitination of the target proteins - E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...
The Proteasome01:13

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. This involves participation of a series of enzymes including— E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3 (ubiquitin...
The Proteasome02:18

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important amongst these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. A series of enzymes carry out the ubiquitination of the target proteins - E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Bone Disorders01:29

Bone Disorders

Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...

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Related Experiment Video

Updated: May 21, 2026

Cell Subtype-specific Analysis of Neuronal Membrane Proteasome in Somatosensory Neurons
09:27

Cell Subtype-specific Analysis of Neuronal Membrane Proteasome in Somatosensory Neurons

Published on: October 10, 2025

Proteasome inhibitors and bone disease.

Ya-Wei Qiang1, Christoph J Heuck, John D Shaughnessy

  • 1Myeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. yqiang@uams.edu

Seminars in Hematology
|June 26, 2012
PubMed
Summary

Proteasome inhibitors (PIs) enhance bone formation by promoting osteoblast differentiation and suppress bone breakdown by inhibiting osteoclasts in multiple myeloma (MM). This dual action helps combat the bone disease associated with MM. Keywords: proteasome inhibitors, multiple myeloma, bone disease, osteoblasts, osteoclasts.

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Published on: September 26, 2016

Area of Science:

  • Oncology
  • Bone Biology
  • Pharmacology

Background:

  • Multiple myeloma (MM) causes bone disease via increased osteoclast activity and decreased osteoblast function.
  • MM inhibits bone formation by suppressing Wnt/β-catenin signaling and altering the RANKL/OPG axis.
  • Mesenchymal stem cell (MSC) differentiation into osteoblasts is crucial for bone health.

Purpose of the Study:

  • To review the mechanisms by which proteasome inhibitors (PIs) stimulate bone formation.
  • To discuss how PIs suppress bone resorption in the context of MM bone disease.
  • To highlight the therapeutic potential of PIs in managing MM-associated bone complications.

Main Methods:

  • Review of existing literature on proteasome inhibitors, Wnt/β-catenin signaling, osteoclastogenesis, and osteoblastogenesis.
  • Analysis of pathways regulated by PIs, including NF-κB and Bim.
  • Examination of the RANKL/OPG axis modulation by PIs.

Main Results:

  • Proteasome inhibitors (PIs), like bortezomib (Bz), activate the Wnt/β-catenin pathway, promoting MSC differentiation into osteoblasts.
  • PIs suppress osteoclastogenesis through various pathways, including NF-κB and Bim.
  • Clinical data show PIs increase bone formation markers and decrease bone resorption markers in MM patients.

Conclusions:

  • PIs demonstrate a dual role in managing MM bone disease by enhancing osteoblast function and inhibiting osteoclast activity.
  • The Wnt/β-catenin pathway and RANKL/OPG axis are key targets for PI-mediated bone protection in MM.
  • PIs represent a promising therapeutic strategy for mitigating bone lesions in multiple myeloma.