Stemness-associated Genes
Stemness-associated Genes - Related Videos
02:35
siRNA-Mediated Gene Silencing in Neural Stem Cells
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2025
This video demonstrates the use of small interfering RNA (siRNA) to silence specific genes of interest in neural stem cells and differentiate them into desired cell types using appropriate differentiation medium. This procedure enables the study of the critical role of specific genes in the differentiation process of neural stem cells.
11:16
Preparation and Gene Modification of Nonhuman Primate Hematopoietic Stem and Progenitor Cells
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Cited by 9 •
2019
The goal of this protocol is to isolate nonhuman primate CD34+ cells from primed bone marrow, to gene-modify these cells with lentiviral vectors, and to prepare a product for infusion into the autologous host. The total protocol length is approximately 48 h.
12:19
In vitro and in vivo Bioluminescence Reporter Gene Imaging of Human Embryonic Stem Cells
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Cited by 28 •
2008
With the growing interest in stem cell therapies, molecular imaging techniques are ideal for monitoring stem cell behavior after transplantation. Luciferase reporter genes have enabled non-invasive, repetitive assessment of cell survival, location, and proliferation in vivo. This video will demonstrate how to track hESC proliferation in a living mouse.
08:32
CRISPR/Cas9 Gene Editing of Hematopoietic Stem and Progenitor Cells for Gene Therapy Applications
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Cited by 6 •
2022
The present protocol describes an optimized hematopoietic stem and progenitor cell (HSPC) culture procedure for the robust engraftment of gene-edited cells in vivo.
22:06
Derivation of Hematopoietic Stem Cells from Murine Embryonic Stem Cells
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Cited by 7 •
2007
This protocol details the derivation of transplantable hematopoietic stem cells from mouse embryonic stem cells (ESC) and their subsequent injection into lethally irradiated recipient mice. Briefly, ESC are differentiated as embryoid bodies, which are then infected with retroviral HoxB4 and co-cultured with OP9 stromal cells and hematopoietic cytokines.
FAQs
Their activity contributes to a regulatory balance rather than enforcing a single permanent cell state. Depending on the transcriptional networks and signaling conditions present, tumor cells may continue proliferating, enter a relatively quiescent state, or shift toward differentiation. This flexibility allows cancer cell populations to adjust their behavior as conditions change within the tumor.
Dysregulated expression can stabilize cancer stem-like states and support continued tumor maintenance. It may also increase the population’s ability to adapt when local conditions change, including shifts that favor survival of only a subset of cells. Consequently, abnormal activity in these genes can connect cellular state regulation with persistence of malignant populations.
Different cells within one tumor may display different levels or combinations of stemness-associated activity. These patterns can reflect distinct cellular states, varying degrees of plasticity, or transitions between proliferation, quiescence, and differentiation. A measured signal therefore describes the composition and state distribution of the sampled population, rather than necessarily identifying one uniform tumor cell type.
Researchers can assess their activity with transcriptomic or other molecular assays that measure gene-expression patterns in tumor samples or cancer cell populations. The resulting profiles help determine whether stemness-associated programs are present and how strongly they vary across samples or subpopulations. Interpretation is most useful when linked to tumor heterogeneity, progression, or treatment response.
Expression patterns can be used to characterize populations that retain cancer stem-like features during disease analysis. Comparing these patterns with treatment-related outcomes may reveal associations between stemness programs and persistence of resistant cells. This information can help researchers investigate which cellular states remain after treatment and evaluate whether disrupting tumor-maintaining programs could reduce their survival.
Changes in their activity provide molecular evidence of cancer cell plasticity, meaning the capacity of cells to shift between functional states. Profiling these changes can support studies of disease progression and help explain how residual tumor populations contribute to recurrence. The same measurements also provide a basis for evaluating approaches designed to interfere with tumor maintenance and relapse.