Human PTEN Knockout Cell Line-HCT116
Cat.No. : CSC-RT0045
Host Cell: HCT116 Target Gene: PTEN
Size: 1x10^6 cells/vial, 1mL Validation: Sequencing
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Cell Line Information
Cell Culture Information
Safety and Packaging
| Cat. No. | CSC-RT0045 |
| Cell Line Information | HCT116-PTEN (+/-) is a cell line with a heterozygous knockout of human PTEN |
| Target Gene | PTEN |
| Host Cell | HCT116 |
| Species | Human |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
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Background
Case Study
Applications
PTEN, or phosphatase and tensin homolog, is a key tumor suppressor gene located on chromosome 10q23.3. Its gene product, PTEN protein, is a dual-specificity phosphatase that dephosphorylates phosphatidylinositol (3,4,5)-triphosphate (PIP3) to phosphatidylinositol (4,5)-bisphosphate (PIP2). This dephosphorylation activity plays a key role in negatively regulating the PI3K/AKT signaling pathway, which is essential for processes such as cell growth, proliferation, survival, and metabolism.
Mutations or loss of function in the PTEN gene are often associated with various cancers, including glioblastoma, endometrial cancer, prostate cancer, and breast cancer. Such mutations result in decreased or absent PTEN protein function, which leads to uncontrolled activation of the PI3K/AKT pathway and promotes carcinogenesis. In addition to cancer, PTEN mutations have been associated with several other pathological conditions, such as Cowden syndrome, Lhermitte-Duclos disease, and autism spectrum disorders. Due to its multifaceted roles, PTEN is a focus of research in cancer biology and therapeutic development. Understanding its regulatory mechanisms and interactions with other cellular proteins could pave the way for new cancer treatments and interventions.
PTEN (phosphatase and tensin homolog), a tumor suppressor that negatively regulates the PI3K signaling pathway, is the second most frequently mutated gene in human cancer. Reduced PTEN expression is associated with colorectal cancer metastasis and poor patient survival. Three-dimensional (3D) multicellular spheroid models have been hypothesized to bridge the gap between 2D cell models and animal 10 models for cancer research and drug discovery. However, little is known about the effects of PTEN loss on invasion of colon cancer spheroid cells through 3D extracellular matrices, and current technologies are limited in their ability to study in vitro 3D cell models in real time.
Here, the researchers studied the migration and invasion behavior of the colon cancer cell line HCT116 and its PTEN-/- isogenic cell line using three different in vitro assays, wound healing, Transwell invasion, and a label-free single-cell 3D2 invasion assay enabled by a resonant waveguide grating (RWG) biosensor. Optical microscopy and RWG imaging revealed that PTEN loss affected spheroid formation of HCT116 cells at high seeding density and accelerated spontaneous metastasis from spheroids to substrate surfaces. In vitro migration and invasion assays showed that PTEN knockout increased the 2D migration speed of HCT116 cells and the invasion rate of single cells through Matrigel or spheroid cells through 3D Matrigel. In addition, PI3K inhibitor treatment significantly reduced the invasiveness of both cell lines. This study shows that PTEN knockout enhances the invasiveness of colorectal cancer spheroid cells through 3D extracellular matrices, and label-free single-cell analysis is very useful for studying cancer cell invasiveness, especially using 3D cell models.
Figure 1. PTEN deletion increases the spontaneous transfer of cells in spheroid to the bare biosensor surface. (a, b) Light microscopic image of the wide-type HCT116 cells (a) or PTEN knockout cell-HCT116 (PTEN-/- cells) (b). (c, d) Corresponding DMR image of the wide-type (c) or PTEN-/- cells (d). (e) The adhesion area at 24 hrs versus cell types. (f) The representative real-time DMR of the wide-type cells at single pixelated position along the dotted line indicated in (c). (g) The representative real-time DMR of the PTEN-/- cells at single pixelated position along the dotted line indicated in (d). (h) The total adhesion events at 24 hrs versus cell types. (i) The distribution of the adhesion time to reach 200 pm versus cell types. (Chandrasekaran S, et al., 2015)
The PTEN (phosphatase and tensin homolog) gene is an important tumor suppressor that is frequently studied in cancer research. HCT116 is a widely used human colorectal cancer cell line. When PTEN is knocked out in HCT116 cells, the resulting cell line becomes a valuable tool for a variety of biomedical and cancer research applications. Here are some key applications:
Cancer Research: PTEN is a tumor suppressor gene and its knockout in HCT116 cells provides a valuable model for understanding its role in cancer progression and development. Researchers can study the downstream effects of PTEN loss, such as uncontrolled cell growth and survival, which are hallmarks of cancer.
Drug Screening: PTEN knockout HCT116 cells can be used to screen for drugs that target pathways activated by PTEN loss. This can aid in the development of targeted therapies, especially for cancers where PTEN is frequently mutated or lost.
Cell Signaling Studies: PTEN is involved in the PI3K/AKT signaling pathway, which is critical for cell growth and survival. By using PTEN knockout HCT116 cells, researchers can dissect the pathway in greater detail, identify new components, and understand the broader impact of its dysregulation.
Genetic Studies: These cells can serve as a tool to study genetic networks and interactions affected by PTEN loss.
Metastasis studies: The PTEN knockout HCT116 cell line can help researchers study how PTEN loss contributes to cancer metastasis. Studies can be performed to examine changes in cell motility, invasiveness, and adhesion.
For research use only. Not intended for any clinical use.
