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The stem cell niche is the dynamic microenvironment where stem cells reside. Inside these niches, the cells may remain undifferentiated, undergo high self-renewal, or become lineage-specific progenitors. Stem cells coexist with other niche cells, such as stromal cells. They also interact closely with the ECM. Cell-cell and cell-matrix communication occur via adhesion molecules or soluble factors that signal the stem cells and determine their fate. Stromal cells also provide survival signals to...
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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.
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The extracellular matrix or ECM holds cells together to form a tissue and allows the cells within the tissue to communicate. ECM comprises proteins such as fibronectin, collagen, laminin, etc. The most abundant protein in this space is collagen. Collagen fibers are interwoven with carbohydrate-containing protein molecules called proteoglycans. ECM allows cell migration and provides a structural scaffold at cell adhesion that anchors the cell when the extracellular matrix proteins interact with...
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An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
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Cell-matrix interface regulates dormancy in human colon cancer stem cells.

Yuki Ohta1, Masayuki Fujii1, Sirirat Takahashi1

  • 1Department of Organoid Medicine, Sakaguchi Laboratory, Keio University School of Medicine, Tokyo, Japan.

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|July 7, 2022
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Cancer stem cells (CSCs) can cause relapse after chemotherapy. We identified dormant LGR5+ CSCs expressing p27 and COL17A1, which maintain dormancy. Inhibiting YAP signaling prevents relapse by blocking CSCs from exiting dormancy.

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Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Stem Cell Research

Background:

  • Cancer relapse post-chemotherapy is a major cause of mortality.
  • Cancer stem cells (CSCs) are implicated in relapse, but their dynamics are poorly understood due to limited experimental platforms.
  • Existing research lacks spatiotemporal resolution to track CSC behavior during treatment.

Purpose of the Study:

  • To develop a live genetic lineage-tracing system for prospective analysis of CSC dynamics.
  • To identify mechanisms of chemoresistance and cancer relapse in colorectal cancer.
  • To explore therapeutic strategies targeting CSC dormancy.

Main Methods:

  • Developed a live genetic lineage-tracing system for human colorectal cancer organoids.
  • Utilized intravital imaging to track individual cell behavior longitudinally.
  • Performed transcriptome analysis and gene knockout (COL17A1) experiments.
  • Investigated the role of FAK-YAP signaling in CSC dormancy.

Main Results:

  • Identified dormant LGR5+ cancer stem cells (CSCs) expressing p27 in a chemo-naive state.
  • Demonstrated persistence and clonal expansion of LGR5+p27+ CSCs during chemotherapy.
  • Found COL17A1 upregulation in dormant CSCs, crucial for maintaining dormancy via the cell-matrix interface.
  • Showed that chemotherapy disrupts COL17A1 and activates FAK-YAP signaling, breaking dormancy.
  • YAP signaling inhibition prevented CSCs from exiting dormancy and delayed tumor regrowth.

Conclusions:

  • Dormant LGR5+p27+ CSCs, maintained by COL17A1 and the cell-matrix interface, are responsible for chemotherapy resistance and relapse.
  • Chemotherapy-induced FAK-YAP activation triggers CSCs to exit dormancy.
  • Targeting YAP signaling offers a promising therapeutic strategy to prevent colorectal cancer relapse.