Panoply™ Human SMO Knockdown Stable Cell Line

Name: Panoply™ Human SMO Knockdown Stable Cell Line
SKU: CSC-DC014764
Availability: InStock

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

Cat. No. : CSC-DC014764

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

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Gene Information

Cat. No.	CSC-DC014764
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	SMO
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	SMO smoothened, frizzled family receptor [ Homo sapiens ]
Gene Symbol	SMO
Synonyms	Gx; SMOH; FZD11
Gene ID	6608
Uni Prot ID	A4D1K5
m RNA Refseq	NM_005631.4
Protein Refseq	NP_005622.1
Chromosome Location	7q32.3
Function	G-protein coupled receptor activity; PDZ domain binding; Wnt-activated receptor activity; Wnt-protein binding; drug binding; patched binding; protein binding;
Pathway	Basal cell carcinoma, organism-specific biosystem; Basal cell carcinoma, conserved biosystem; Class B/2 (Secretin family receptors), organism-specific biosystem; GPCR ligand binding, organism-specific biosystem; GPCRs, Other, organism-specific biosystem; Hedgehog Signaling Pathway, organism-specific biosystem; Hedgehog signaling events mediated by Gli proteins, organism-specific biosystem;
MIM	601500

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Hedgehog (Hh) signaling promotes castration-resistant prostate cancer by supporting the development and growth of androgen-independent prostate cancer cells. However, its role in neuroendocrine prostate cancer (NEPC) has been less well-studied. Here, researchers evaluated the expression of key genes involved in Hh signaling in prostate cancer and explored the potential role of smooth muscle cell (SMO) in the pathogenesis of NEPC. They analyzed six public datasets, each containing prostate adenocarcinoma (AdPC) and NEPC cases, to compare the differential messenger RNA (mRNA) expression of six canonical Hh signaling genes. Results showed that SMO mRNA levels were significantly downregulated in NEPC samples across all six public datasets, while SMO mRNA levels were significantly downregulated in AdPC samples. SMO protein loss was observed in 100% of NEPC samples, but only in 9% of high-grade AdPC samples. GSEA results showed that SMO loss was closely associated with AR signaling activity. Stable SMO knockdown significantly attenuated AR signaling and suppressed AR expression, whereas Gli1 overexpression partially reversed the inhibitory effects of SMO knockdown on AR signaling and expression in LNCaP and C4-2B cells. These results suggest that SMO deficiency is a hallmark of NEPC and that immunohistochemical (IHC) detection of SMO may aid pathologists in diagnosing NEPC. SMO deficiency may contribute to the pathogenesis of NEPC by modulating AR signaling.

Here, researchers established stable SMO knockdown LNCaP and C4-2B cell lines to evaluate the effect of SMO loss on AR signaling. As shown in Figures 1A and B, AR and PSA expression was reduced in SMO knockdown cells compared with control cells, while the expression levels of NE markers were not significantly different.

Figure 1. Knockdown of SMO inhibits AR pathway activity and reduces AR expression. (Wang L, et al., 2021)

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