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Panoply™ Human ERBB2 Over-expressing Stable Cell Line

Panoply™ Human ERBB2 Over-expressing Stable Cell Line

Cat.No. :  CSC-SC005027 Host Cell:  HEK293 (CHO and other cell types are also available)

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Gene Informationn

Cat. No. CSC-SC005027
Description Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level.
Gene ERBB2
Gene Species Homo sapiens (Human)
Host Cell HEK293 (CHO and other cell types are also available)
Stability Validated for at least 10 passages
Application

1. Gene expression studies

2. Signaling pathway research

3. Drug screening and toxicology

4. Disease research

Quality Control Negative for bacteria, yeast, fungi and mycoplasma.
Size Form 2 × 10^6 cells / vial
Shipping Dry Ice
Storage Liquid nitrogen
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.
Gene Name
Gene Symbol
Synonyms
Gene Description
Gene ID
UniProt ID
mRNA Refseq
Protein Refseq
Chromosome Location
Function
Pathway
MIM
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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Breast cancer is a heterogeneous disease, classified into different subtypes with varying clinical prognoses and treatment strategies. Although ERBB3/HER3 and its partner ERBB2/HER2 are expressed at low levels in basal-like/triple-negative breast cancer, stratified analysis of basal-like breast cancer patients based on ERBB3 mRNA expression levels revealed that higher ERBB3 expression levels were associated with shorter recurrence-free survival. In vitro analyses showed that activation of the NRG1/ERBB3/ERBB2 axis significantly induced anchorage-independent growth in a basal-like/triple-negative breast cancer cell model without significantly affecting cell proliferation, differentiation, and migration in adhesion. Overall, these data suggest that ERBB2/ERBB3 plays an oncogenic role in basal-like/triple-negative breast cancer, suggesting that neutralizing ERBB2/ERBB3 could be a potential treatment strategy for these breast cancer subtypes, where current treatment options are very limited.

Approximately 25% of HER2-negative triple-negative breast cancers in primary tumors transform into HER2-low-expressing tumors in recurrent tumors, maintaining the same cancer phenotype. Here, the study suggests that loss of cell adhesion may promote ERBB2 upregulation. Researchers also used stably ERBB2-overexpressing MCF10A cells (MCF10A-HER2) to evaluate the role of the NRG1β/ERBB3/ERBB2 axis in basal-like cells with increased expression of ERBB2. Compared to untreated control cells, administration of NRG1β to ERBB2-overexpressing MCF10A cells induced an increase in the number and size of spheroid, which was significantly inhibited by pertuzumab, but not by trastuzumab in combination (Figures 1a-c). Overall, these data suggest that pertuzumab effectively inhibits NRG1β-induced basal-like breast cell growth even with ERBB2 upregulation.

Figure 1. Administration of NRG1β promotes growth in non-adherent conditions in basal-like/triple-negative breast cells engineered with HER2 overexpression.Figure 1. Administration of NRG1β promotes growth in non-adherent conditions in basal-like/triple-negative breast cells engineered with HER2 overexpression. (Miano C, et al., 2022)

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