Panoply™ Human CYP11A1 Knockdown Stable Cell Line

Name: Panoply™ Human CYP11A1 Knockdown Stable Cell Line
SKU: CSC-DC003935
Availability: InStock

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

Cat. No. : CSC-DC003935

Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR

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Cell Line Information

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Gene Information

Cat. No.	CSC-DC003935
Description	Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free.
Target Gene	CYP11A1
Host Cell	HEK293 (Hela and other cell types are also available)
Host Cell Species	Homo sapiens (Human)
Applications	(1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models
Size	>1 × 10⁶ cells / vial
Stability	Validated for at least 10 passages
Validation	Real-Time RCR
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid Nitrogen
Shipping	Dry Ice

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	CYP11A1 cytochrome P450, family 11, subfamily A, polypeptide 1 [ Homo sapiens ]
Gene Symbol	CYP11A1
Synonyms	CYP11A; CYPXIA1; P450SCC
Gene Description	cytochrome P450, family 11, subfamily A, polypeptide 1
GeneID	1583
Uni ProtID	P05108
mRNA Refseq	NM_000781.2
Protein Refseq	NP_000772.2
Chromosome Location	15q23-q24
Function	cholesterol binding; cholesterol monooxygenase (side-chain-cleaving) activity; cholesterol monooxygenase (side-chain-cleaving) activity; electron carrier activity; heme binding; iron ion binding;
Pathway	Biological oxidations, organism-specific biosystem; Cytochrome P450 - arranged by substrate type, organism-specific biosystem; Endogenous sterols, organism-specific biosystem; Glucocorticoid & Mineralcorticoid Metabolism, organism-specific biosystem; Metabolism, organism-specific biosystem;
MIM	118485

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Both cholesterol and Helicobacter pylori (H. pylori) are risk factors for gastric cancer (GC). Here, researchers found that H. pylori induces mitochondrial cholesterol accumulation and promotes GC cell proliferation while inhibiting apoptosis in a cholesterol-dependent manner. Through metabolomics and transcriptomic sequencing analyses, the researchers identified CYP11A1 as the key molecule mediating H. pylori-induced cholesterol accumulation. Functional experiments in vitro and in vivo demonstrated that cholesterol promotes GC cell proliferation and inhibits apoptosis. Mechanistic studies revealed that the cytotoxin-associated gene A (CagA) interacts with CYP11A1, causing the translocation of CYP11A1 out of the mitochondria, which subsequently triggers mitochondrial cholesterol accumulation. Knockdown of CYP11A1 exacerbated cholesterol accumulation and recapitulated the effects of cholesterol on GC cells in a cholesterol-dependent manner. Furthermore, both CYP11A1 knockdown and H. pylori infection inhibited mitophagy, thereby maintaining mitochondrial homeostasis. H. pylori promotes GC progression via the CagA/CYP11A1-mitoCHO axis. This study confirms that H. pylori facilitates GC progression through cholesterol-related pathways; thus, H. pylori eradication remains significant for improving the prognosis of GC patients.

Wild-type Helicobacter pylori (H. pylori^WT) can promote gastric cancer (GC) progression by upregulating cholesterol levels via CYP11A1. However, it remains unclear whether CYP11A1 influences GC progression through cholesterol. To investigate this, researchers performed CCK-8, colony formation, and EdU assays on treated GC cells (Figure 1A–H). The results showed that cell proliferation was enhanced in CYP11A1-knockdown GC cells, an effect that was reversed by cholesterol depletion using statins (Figure 1A, C, E, G). Conversely, CYP11A1 overexpression inhibited GC cell proliferation, an inhibitory effect that was reversed by cholesterol supplementation (Figure 1B, D, F, H).

Figure 1. CYP11A1 impacted the proliferation and apoptosis of GC by regulating cholesterol. (Zhang Z, et al., 2024)

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