Panoply™ Human AKT1 Knockdown Stable Cell Line

Name: Panoply™ Human AKT1 Knockdown Stable Cell Line
SKU: CSC-DC000464
Availability: InStock

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

Cat. No. : CSC-DC000464

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

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Gene Information

Cat. No.	CSC-DC000464
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	AKT1
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	AKT1 v-akt murine thymoma viral oncogene homolog 1 [ Homo sapiens ]
Gene Symbol	AKT1
Synonyms	AKT; PKB; RAC; PRKBA; PKB-ALPHA; RAC-ALPHA
Gene Description	v-akt murine thymoma viral oncogene homolog 1
GeneID	207
Uni ProtID	B0LPE5
mRNA Refseq	NM_001014431.1
Protein Refseq	NP_001014431.1
Chromosome Location	14q32.32
Function	ATP binding; ATP binding; enzyme binding; identical protein binding; kinase activity; nitric-oxide synthase regulator activity; phosphatidylinositol-3,4,5-trisphosphate binding; phosphatidylinositol-3,4-bisphosphate binding; protein binding; protein kinase C binding; protein kinase activity; protein serine/threonine kinase activity; protein serine/threonine kinase activity;
Pathway	AKT phosphorylates targets in the cytosol, organism-specific biosystem; AKT phosphorylates targets in the nucleus, organism-specific biosystem; AKT-mediated inactivation of FOXO1A, organism-specific biosystem; AMPK signaling, organism-specific biosystem; Activation of BAD and translocation to mitochondria, organism-specific biosystem; Activation of BH3-only proteins, organism-specific biosystem; Acute myeloid leukemia, organism-specific biosystem;
MIM	164730

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Osteosarcoma (OS) is closely associated with the dysregulation of multiple intracellular signaling pathways, especially the PI3K/Akt signaling pathway. It has been reported that HSP90 is responsible for the stabilization of phosphorylated Akt, and both AKT1 and HSP90 are upregulated in osteosarcoma. Here, researchers showed that both AKT1 and HSP90 mRNA and protein levels are upregulated in osteosarcoma tissues and cells; AKT1 gene knockdown significantly inhibited osteosarcoma cell viability. HSP90 gene knockdown inhibited AKT1 phosphorylation, decreased Ki-67 and Vimentin protein levels, increased p21 and E-cadherin protein levels, and inhibited osteosarcoma cell proliferation and migration. AKT1 overexpression had the opposite effect and significantly attenuated the effects of HSP90 gene knockdown. miR-485-5p targets the 3′-UTR of both AKT1 and HSP90, inhibiting their expression. miR-485-5p overexpression significantly decreased AKT1, HSP90, and Ki-67 protein levels, increased E-cadherin protein levels, and inhibited osteosarcoma cell proliferation and migration. In summary, HSP90 gene knockdown blocks AKT1 phosphorylation through the PI3K/AKT pathway, thereby inhibiting osteosarcoma cell proliferation and migration. miR-485-5p binds to the 3′-UTR of both HSP90 and AKT1, inhibiting their expression and thus exerting a tumor-suppressive effect in osteosarcoma.

Based on the important role of the PI3K/AKT pathway in osteosarcoma (OS), researchers first examined the expression levels of key proteins in the PI3K/AKT pathway in osteosarcoma tissue samples and cell lines (U2OS and MG63). The results showed that the expression levels of PI3K, AKT1, and p-AKT1 proteins were significantly higher in osteosarcoma tissue samples and the two osteosarcoma cell lines compared to normal tissue samples and cells (Figure 1a, b). Consistent with this, AKT1 mRNA expression was also higher in osteosarcoma tissue samples and cells than in normal tissue samples and cell lines (Figure 1c, d). To verify the cellular function of AKT1, researchers constructed AKT1 knockdown U2OS and MG63 cells (Figure 1e). The results showed that the viability of AKT1 knockdown U2OS and MG63 cells was significantly reduced (Figure 1f). In summary, AKT1 is upregulated in osteosarcoma. AKT1 gene knockdown may inhibit the growth of osteosarcoma cells.

Figure 1. AKT1 expression in osteosarcoma (OS) tissues and cells and its cellular functions. (Liu Q, et al., 2020)

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