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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...
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,...
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,...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
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...

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Related Experiment Video

Updated: Jun 4, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

NAT10-dependent N4-acetylcytidine reprograms R-loops and promotes cancer stem cell growth.

Xujia Wu1, Donghai Wang2, Suchet Taori1

  • 1Hillman Cancer Center, University of Pittsburgh Medical Center, Pittsburgh, PA, USA.

Cell Reports
|June 2, 2026
PubMed
Summary

Glioblastoma stem cells use R-loops to sustain self-renewal. Targeting the NAT10 protein and its ac4C modification on R-loops inhibits cancer growth, offering a potential therapeutic strategy.

Keywords:
CP: cancerCP: neuroscienceEGR1NAT10R-loop remodelinac(4)Ccancer stem cellepitranscriptomicsglioblastomaglioblastoma stem cell

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Combined Conditional Knockdown and Adapted Sphere Formation Assay to Study a Stemness-Associated Gene of Patient-derived Gastric Cancer Stem Cells
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Combined Conditional Knockdown and Adapted Sphere Formation Assay to Study a Stemness-Associated Gene of Patient-derived Gastric Cancer Stem Cells

Published on: May 9, 2020

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Last Updated: Jun 4, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

Combined Conditional Knockdown and Adapted Sphere Formation Assay to Study a Stemness-Associated Gene of Patient-derived Gastric Cancer Stem Cells
09:24

Combined Conditional Knockdown and Adapted Sphere Formation Assay to Study a Stemness-Associated Gene of Patient-derived Gastric Cancer Stem Cells

Published on: May 9, 2020

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • R-loops are RNA:DNA hybrids involved in gene regulation.
  • Cancer cells, particularly glioblastoma stem cells (GSCs), exploit R-loops for malignancy.
  • The precise role of R-loops in GSC self-renewal and the underlying mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the role of R-loops in glioblastoma stem cell (GSC) self-renewal and malignancy.
  • To identify proteins that bind to R-loops in GSCs and elucidate their function.
  • To explore therapeutic strategies targeting R-loops in glioblastoma.

Main Methods:

  • Genome-wide mapping of R-loops in GSCs and control cells.
  • Identification and characterization of R-loop-binding proteins, including NAT10.
  • Analysis of ac4C modification on RNA within R-loops.
  • In vitro and in vivo experiments assessing the impact of NAT10 inhibition on GSC behavior and tumor growth.

Main Results:

  • GSCs exhibit significantly higher R-loop activity compared to differentiated cells.
  • R-loops accumulate at promoter-proximal regions in GSCs, correlating with active transcription and open chromatin.
  • N-acetyltransferase 10 (NAT10) binds to R-loops in GSCs and catalyzes ac4C deposition, stabilizing R-loops and promoting self-renewal via EGR1.
  • NAT10 inhibition or pharmacological targeting of ac4C-modified R-loops suppresses GSC proliferation and tumor growth.

Conclusions:

  • R-loops are critical for glioblastoma stem cell self-renewal and malignancy.
  • NAT10-mediated ac4C modification of R-loops is a key mechanism sustaining GSC stemness.
  • Targeting NAT10 and ac4C-modified R-loops represents a promising therapeutic avenue for glioblastoma.