Hct116 Cell Line
Hct116 Cell Line - Related Videos
10:33
Assessing Cell Viability and Death in 3D Spheroid Cultures of Cancer Cells
0 Views •
Cited by 34 •
2019
Here, we present several simple methods for evaluating viability and death in 3D cancer cell spheroids, which mimic the physico-chemical gradients of in vivo tumors much better than the 2D culture. The spheroid model, therefore, allows evaluation of the cancer drug efficacy with improved translation to in vivo conditions.
07:10
Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus
0 Views •
2025
This protocol describes an in vitro system to model de novo lytic infection of Kaposi's sarcoma-associated herpesvirus using BAC16-derived virions. The method enables investigation of early viral replication and dissemination. Infectious virus production is quantified by GFP-based infectious units assays and real-time PCR of encapsidated viral genomes.
10:04
Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
0 Views •
2025
This protocol describes the in vivo reprogramming of mouse cancer cells into type 1 dendritic-like cells within the tumor microenvironment through enforced expression of the transcription factors PU.1, IRF8, and BATF3.
22:06
Derivation of Hematopoietic Stem Cells from Murine Embryonic Stem Cells
0 Views •
Cited by 8 •
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.
02:47
Human ES cells: Starting Culture from Frozen Cells
0 Views •
2006
Here we demonstrate how our lab begins a HuES human embryonic stem cell line culture from a frozen stock.
FAQs
Mismatch-repair deficiency allows replication-associated errors to persist, producing microsatellite instability, or MSI, in HCT116 cells. MSI changes the mutation patterns present in the model, so experiments involving DNA repair, mutation-sensitive pathways, or treatment response must interpret results in light of that genetic background. This feature makes the line useful for connecting repair defects with cancer-cell behavior.
Adherent epithelial-like growth gives HCT116 cultures a consistent cellular context for examining proliferation, cell-cycle regulation, and apoptosis. Because the cells grow attached under controlled laboratory conditions, researchers can relate changes in cell behavior to experimental perturbations rather than to a fundamentally different growth format. The phenotype therefore supports reproducible studies of colorectal cancer-associated mechanisms.
The well-characterized genetics of HCT116 provide a defined background in which gene-editing approaches can test molecular mechanisms. Researchers can alter or examine a selected genetic factor and then evaluate consequences for proliferation, DNA repair, cell-cycle control, apoptosis, or signaling. This links a specific genomic change to a measurable cancer-related phenotype and can help validate a therapeutic target.
Treatment results should be interpreted against the line’s mismatch-repair deficiency, microsatellite instability, and defined genetic background. These features can shape mutation patterns and experimental responses, meaning that a compound effect may reflect interactions with particular DNA-repair or tumor-signaling states. HCT116 therefore helps reveal mechanisms of response, but findings remain tied to the model’s molecular context.
Maintaining HCT116 for experiments requires controlled laboratory culture conditions that preserve its adherent epithelial-like growth and reliable proliferation. A study can then introduce the planned molecular or compound perturbation and compare resulting changes in growth, cell-cycle regulation, apoptosis, DNA repair, or signaling. Keeping the culture context consistent improves interpretation of differences between experimental conditions.
Researchers apply HCT116 to questions spanning DNA repair, cell-cycle regulation, apoptosis, tumor-associated signaling, and anticancer-compound response. The model is especially useful when a study needs both a colorectal carcinoma context and a genetically characterized system. Results can connect a molecular mechanism with a cancer-relevant cellular outcome, supporting early evaluation of biological hypotheses and therapeutic targets.
Target-validation studies can use HCT116 to test whether changing a candidate molecular factor alters a cancer-relevant phenotype. Researchers may examine effects on proliferation, DNA repair, cell-cycle regulation, apoptosis, or tumor-associated signaling, then relate those findings to anticancer-compound responses. This provides a mechanistic basis for judging whether the target merits further investigation.