Related Experiment Video

Updated: May 28, 2026

Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses
10:13

Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses

Published on: May 6, 2019

Microparticle-associated nucleic acids mediate trait dominance in cancer

Ritu Jaiswal1, Joyce Gong, Shwetha Sambasivam

  • 1Sydney Medical School and Bosch Institute, University of Sydney,Sydney, Australia.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|October 4, 2011
PubMed

Insights

Microparticles (MPs) transfer drug resistance proteins like P-glycoprotein (P-gp) between cancer cells, enabling drug resistance. This intercellular transfer provides a novel mechanism for cancer treatment failure.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Multidrug resistance (MDR) is a significant challenge in cancer therapy, leading to treatment failure.
  • MDR arises from the overexpression of efflux transporters such as P-glycoprotein (P-gp) and multidrug resistance-associated protein 1 (MRP1).
  • These transporters reduce intracellular drug accumulation, rendering cancer cells unresponsive to treatment.

Purpose of the Study:

  • To investigate a novel, non-genetic mechanism of multidrug resistance acquisition in cancer cells.
  • To determine the role of microparticles (MPs) in the intercellular transfer of drug resistance factors.
  • To explore the implications of MP-mediated drug resistance in clinical oncology.

Main Methods:

  • Isolation of microparticles (MPs) from multidrug-resistant (MDR) leukemia and breast cancer cells.
  • Co-culture of MDR-derived MPs with drug-sensitive cancer cells.
  • Assessment of P-glycoprotein (P-gp) transfer via direct immunolabeling.
  • Analysis of acquired transcripts and regulatory microRNAs using quantitative real-time PCR.

Main Results:

  • MDR-derived MPs were shown to incorporate nucleic acids.
  • MPs successfully transferred P-gp to drug-sensitive recipient cells, conferring MDR.
  • Recipient cells exhibited altered transcriptional profiles, reflecting the donor MDR phenotype.
  • This MP-mediated MDR transfer pathway was observed in both hematological and nonhematological malignancies.

Conclusions:

  • Microparticles provide a novel pathway for the intercellular transfer of P-glycoprotein, contributing to multidrug resistance.
  • MPs can reprogram the transcriptional landscape of recipient cells, facilitating the spread of drug resistance.
  • This mechanism has significant implications for understanding cancer treatment failure and the dissemination of acquired traits in clinical oncology.

More Related Videos

CRISPR Gene Editing Tool for MicroRNA Cluster Network Analysis10:40

CRISPR Gene Editing Tool for MicroRNA Cluster Network Analysis

Published on: April 25, 2022

Related Concept Videos

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...