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Related Concept Videos

Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

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Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
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Induced Pluripotent Stem Cells01:06

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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).
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Methods of Nuclear Reprogramming01:24

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Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for...
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The ability of induced pluripotent stem cells or iPSCs to differentiate into most body cell types has stimulated repair and regenerative medicine research over the past few decades. iPSC-derived blood cells, hepatocytes, beta islet cells, cardiomyocytes, neurons, and other cell types can repair injuries or regenerate damaged tissue in diseases such as diabetes and neurodegenerative disorders.
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Related Experiment Video

Updated: Dec 29, 2025

Generation of Induced Pluripotent Stem Cells from Human Melanoma Tumor-infiltrating Lymphocytes
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MiR-302-Mediated Somatic Cell Reprogramming and Method for Generating Tumor-Free iPS Cells Using miR-302.

Shi-Lung Lin1, Jack S Chen1, Shao-Yao Ying2

  • 1WJWU & LYNN Institute for Stem Cell Research, Santa Fe Springs, CA, USA.

Methods in Molecular Biology (Clifton, N.J.)
|February 2, 2020
PubMed
Summary
This summary is machine-generated.

Human induced pluripotent stem cells (iPSCs) can form tumors, but miR-302 microRNA prevents this by regulating cell cycle and tumor suppressor genes, creating safer iPSCs for therapy.

Keywords:
BMI-1CDK2CDK4/6CDKN1ACell cycleCyclin DDND demethylationESCRNAiStem celliPSCmiR-302microRNA (miRNA)p14/p19Arfp16Ink4ap21Cip1/Waf1

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Cell Surface Marker Mediated Purification of iPS Cell Intermediates from a Reprogrammable Mouse Model
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Area of Science:

  • Stem Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Human induced pluripotent stem cells (iPSCs) carry risks of teratoma formation and tumorigenicity.
  • Naturally occurring embryonic stem cells (ESCs) possess self-renewal and pluripotency without tumor risk.
  • Tumor prevention mechanisms in ESCs remain largely uncharacterized.

Purpose of the Study:

  • To investigate the mechanism of tumor suppression in ESCs.
  • To identify factors regulating iPSC tumorigenicity.
  • To develop tumor-free iPSCs for therapeutic applications.

Main Methods:

  • Examined cell cycle gene regulation in embryonic cells.
  • Investigated the role of ESC-specific microRNA (miRNA), miR-302.
  • Analyzed miR-302's effect on cell cycle pathways (cyclin E-CDK2, cyclin D-CDK4/6) and tumor suppressor genes (p16Ink4a, p14/p19Arf).

Main Results:

  • miR-302 co-suppresses cell cycle pathways (G1-S transition) and silences BMI-1, a cancer stem cell marker.
  • miR-302 promotes expression of tumor suppressor genes p16Ink4a and p14/p19Arf.
  • This leads to attenuated cell cycle rates in iPSCs, similar to early embryonic cells, preventing tumor formation.

Conclusions:

  • miR-302 effectively suppresses iPSC tumorigenicity by regulating cell cycle and activating tumor suppressors.
  • miR-302 also initiates DNA methylation, activates ESC-specific genes, and inhibits developmental signaling.
  • A protocol to express miR-302 naturally generates tumor-free iPSCs for safe biological and therapeutic use.