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Panoply™ Human GSTP1 Over-expressing Stable Cell Line

For research use only. Not intended for any clinical use.

Cat. No. :   CSC-SC006722

Host Cell :   HEK293 (CHO and other cell types are also available) Size :   >1x106 frozen cells/vial

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Cell Line Information

Cell Culture Information

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Gene Information

Cat. No. CSC-SC006722
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.
Target Gene GSTP1
Gene Species Homo sapiens (Human)
Host Cell HEK293 (CHO and other cell types are also available)
Host Cell Species Species varies
Applications

1. Gene expression studies

2. Signaling pathway research

3. Drug screening and toxicology

4. Disease research

Size 2 × 10^6 cells / vial
Stability Validated for at least 10 passages
Quality Control Negative for bacteria, yeast, fungi and mycoplasma.
Storage Liquid nitrogen
Shipping Dry Ice
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
Gene Name GSTP1 glutathione S-transferase pi 1 [ Homo sapiens ]
Gene Symbol GSTP1
Synonyms GSTP1; glutathione S-transferase pi 1; FAEES3, GST3; glutathione S-transferase P; GSTP; GSTP1-1; GST class-pi; deafness, X-linked 7; fatty acid ethyl ester synthase III; PI; DFN7; GST3; FAEES3;
Gene ID 2950
Uni Prot ID P09211
m RNA Refseq BC010915
Chromosome Location 11q13.2
Function JUN kinase binding; S-nitrosoglutathione binding; dinitrosyl-iron complex binding; drug binding; glutathione binding; glutathione transferase activity; glutathione transferase activity; kinase regulator activity; nitric oxide binding; protein binding; transferase activity;
Pathway Arachidonate Epoxygenase / Epoxide Hydrolase, organism-specific biosystem; Biological oxidations, organism-specific biosystem; Diurnally regulated genes with circadian orthologs, organism-specific biosystem; Drug metabolism - cytochrome P450, organism-specific biosystem; Drug metabolism - cytochrome P450, conserved biosystem; Glutathione conjugation, organism-specific biosystem; Glutathione metabolism, organism-specific biosystem;
MIM 134660
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Glutathione S-transferase P1 (GSTP1) is a phase II detoxification enzyme, and elevated GSTP1 expression is associated with acquired resistance to anticancer drugs. However, most anticancer drugs are not good substrates for GSTP1, suggesting that GSTP1's contribution to resistance may not depend on its ability to detoxify chemicals or drugs. Here, researchers have discovered a novel mechanism by which GSTP1 protects human breast cancer cells from doxorubicin (ADR)-induced cell death and promotes resistance. GSTP1 protein expression levels are extremely low in the human breast cancer cell line MCF-7, but are higher in ADR-resistant MCF-7/ADR cells. Under ADR treatment, autophagy levels in MCF-7/ADR cells are higher than in MCF-7 cells. Overexpression of GSTP1 in MCF-7 cells using a DNA transfection vector enhances autophagy, while downregulation of GSTP1 in MCF-7/ADR cells via RNA interference reduces autophagy. When autophagy is inhibited, GSTP1-induced ADR resistance is reduced. Researchers discovered that GSTP1 enhances autophagy in MCF-7 cells by interacting with the p110α subunit of phosphatidylinositol-3-kinase (PI3K), thereby inhibiting PI3K/protein kinase B (AKT)/target of rapamycin (mTOR) activity. Proline 123, leucine 160, and glutamine 163 at the C-terminus of GSTP1 are crucial for the interaction between GSTP1 and p110α, as well as subsequent autophagy and drug resistance regulation. In summary, these findings suggest that high levels of GSTP1 maintain ADR resistance in breast cancer cells by promoting autophagy.

Here, researchers reduced GSTP1 expression levels in MCF-7/ADR cells by transfecting plasmids expressing GSTP1 shRNA. As shown in Figure 1d, with GSTP1 RNAi knockdown, the LC3-II/I ratio significantly decreased, while the SQSTM1/p62 level significantly increased. In MCF-7/ADR cells, GSTP1 RNAi also attenuated ADR-stimulated autophagy flux (Figure 1e). As expected, in GSTP1-overexpressing MCF-7 cells, the LC3-II/I ratio increased, and the SQSTM1/p62 level decreased (Figure 1f). Confocal microscopy results showed that GSTP1 overexpression in MCF-7 cells increased the number of LC3 spots and enhanced autophagy flux (Figure 1g). These experiments on both MCF-7 and MCF-7/ADR cells demonstrate that GSTP1 promotes autophagy.

Figure 1. GSTP1 promotes autophagy in breast cancer cells.Figure 1. GSTP1 promotes autophagy in breast cancer cells. (Dong X, et al., 2019)

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