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Related Concept Videos

Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
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,...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...
Enlargement of the Plasma Membrane01:22

Enlargement of the Plasma Membrane

Cell division and enlargement are processes that require precise control. The control ensures that cell division cannot proceed unless the cell has grown to a specific size. A spherical, dividing cell requires an approximately 1.6X increase in its surface area to double its volume. The secretory pathway also has a significant role in cell membrane enlargement. Secretory vesicles that bud off from the Golgi apparatus and later fuse with the plasma membrane during exocytosis are a major source of...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...

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Related Experiment Video

Updated: May 26, 2026

Harnessing the DNA Dye-triggered Side Population Phenotype to Detect and Purify Cancer Stem Cells from Biological Samples
09:57

Harnessing the DNA Dye-triggered Side Population Phenotype to Detect and Purify Cancer Stem Cells from Biological Samples

Published on: May 10, 2017

Self-fueling catalysis-driven membrane destabilization triggers CSC-enriched tumors ablation.

Lin Huang1,2, Basheng Hu3, Guochao Wu2

  • 1Cancer Center, Dongguan Key Laboratory of Precision Diagnosis and Treatment for Tumors, The Tenth Affiliated Hospital, Southern Medical University (Dongguan People's Hospital), Dongguan, 523059, Guangdong, China.

Journal of Nanobiotechnology
|May 24, 2026
PubMed
Summary

This study introduces a novel nanomedicine that eliminates cancer stem cells (CSCs) by disrupting their defenses. The treatment leverages cholesterol depletion and self-fueling catalysis to induce ferroptosis in CSC-enriched tumors.

Keywords:
Cancer stem cellsCholesterol-dependent membrane defensesFerroptosis amplification and propagationHollow mesoporous zinc-copper sulfide nanocapsulesSelf-fueling catalysis

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Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

Related Experiment Videos

Last Updated: May 26, 2026

Harnessing the DNA Dye-triggered Side Population Phenotype to Detect and Purify Cancer Stem Cells from Biological Samples
09:57

Harnessing the DNA Dye-triggered Side Population Phenotype to Detect and Purify Cancer Stem Cells from Biological Samples

Published on: May 10, 2017

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

Area of Science:

  • Biomedical Engineering
  • Nanotechnology
  • Cancer Therapy

Background:

  • Cancer stem cells (CSCs) present a significant therapeutic challenge due to inherent drug resistance and cholesterol-dependent anti-ferroptotic mechanisms.
  • Existing treatments struggle to overcome the protective barriers and resistance pathways employed by CSCs within the tumor microenvironment (TME).

Purpose of the Study:

  • To develop and evaluate a novel nanomedicine, cholesterol oxidase (COD)-loaded hollow mesoporous zinc-copper sulfide (COD@HMZCS-HA), for targeted elimination of CSCs.
  • To investigate the synergistic effects of cholesterol depletion and self-fueling catalysis in overcoming CSC resistance and inducing ferroptosis.

Main Methods:

  • Design of COD@HMZCS-HA nanomedicine for targeted tumor accumulation and release of active components.
  • Utilizing cholesterol oxidase (COD) to deplete cholesterol, dismantle lipid rafts, and inactivate the 7-dehydrocholesterol (7-DHC) brake on lipid peroxidation (LPO).
  • Implementing a self-fueling catalytic cycle involving Cu+, Zn2+, and H2S to generate reactive oxygen species (ROS), relieve hypoxia, and induce intracellular acidification, amplifying LPO.

Main Results:

  • COD@HMZCS-HA effectively depleted cholesterol, destabilized CSC membranes, and sensitized cells to ferroptosis.
  • The self-fueling catalysis amplified LPO, leading to a ferroptotic storm and overcoming hypoxia within the TME.
  • In vitro and in vivo studies demonstrated potent antitumor and antimetastatic efficacy through CSC ablation and disruption of lipid rafts.

Conclusions:

  • The developed self-fueling catalysis strategy effectively overcomes TME hypoxia and cholesterol-dependent anti-ferroptotic defenses.
  • COD@HMZCS-HA nanomedicine offers a promising therapeutic paradigm for the elimination of CSC-enriched tumors by inducing irreversible ferroptosis.
  • This approach bypasses classical resistance pathways, highlighting its potential for improved cancer treatment outcomes.