Cat.No. : CSC-RR0127 Host Cell: Hep3B
| Cat. No. | CSC-RR0127 |
| Description | Hep3B was derived from liver of a 8 year-old black male with hepatocellular carcinoma. The GFP Stable Cell Line-Hep3B constitutively expresses GFP. |
| Host Cell | Hep3B |
| Host Cell Species | Homo sapiens (Human) |
| Stability | Validated for at least 10 passages |
| Reporter Type | Fluorescent protein |
| Application | 1. Gene expression studies 2. Protein localization 3. Drug screening and toxicology 4. Live cell imaging |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Storage | Liquid nitrogen |
| Recommended Medium | Inquiry for instruction of culturing |
| 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 |
Histone modifications are critical for the regulation of chromatin function. Histone modifications affect key biological processes such as gene expression, repair, and the cell cycle by altering the structure and function of chromatin. Researchers used the GFP Stable Cell Line-Hep3B cell line to explore the role of JMJD2A, a demethylating enzyme that is normally overexpressed in tumors, in hepatocellular carcinoma cells, and showed that it accelerated malignant progression. Through an epigenetic mechanism, JMJD2A promoted the expression and maturation of pre-miR372. miR372 formed a new transcript of JMJD2A (JMJD2AΔ) by blocking exon 13-intron-14 editing. jmjd2a inhibited P21 by reducing H3K9me3-dependent JMJD2AΔ (WAF1/Cip1) expression, thereby enhancing Pim1 transcription. Further, JMJD2A promoted the interaction of pRB, CDK2, and CyclinE to drive C-myc transcription and translation by increasing Pim1 expression. This study reveals a novel mechanism of JMJD2A in hepatocellular carcinoma cells, pointing to its potential as a new therapeutic target for hepatocellular carcinoma.
Figure 1. By constructing two stable Hep3B cell lines (pCMV6-AC-GFP control group and pCMV6-AC-GFP-JMJD2A experimental group), the researchers found that JMJD2A significantly promoted the growth of hepatocellular carcinoma cells. the JMJD2A overexpression group showed higher cell proliferation rate, colony formation efficiency, and BrdU positivity. In addition, JMJD2A overexpression significantly increased the weight of xenograft tumors and increased the proportion of undifferentiated cells. This indicated that JMJD2A accelerated the malignant progression of hepatocellular carcinoma cells. (An J, et al., 2019)
A: Hep3B Cell Line's close resemblance to primary hepatocellular carcinoma cells makes it a valuable model for studying the disease's pathogenesis and for evaluating new treatment strategies.
A: While Hep3B Cell Line is a useful model, it is important to consider its limitations, such as potential differences between the cell line and primary tumors, and the need for further validation of research findings using additional models or patient samples.
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GFP Stable Cell Line-Hep3B is easy to culture and requires minimal maintenance, saving me time and effort.
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