Panoply™ Human RAF1 Knockdown Stable Cell Line

Name: Panoply™ Human RAF1 Knockdown Stable Cell Line
SKU: CSC-DC012928
Availability: InStock

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

Cat. No. : CSC-DC012928

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

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Gene Information

Cat. No.	CSC-DC012928
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	RAF1
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	RAF1 v-raf-1 murine leukemia viral oncogene homolog 1 [ Homo sapiens ]
Gene Symbol	RAF1
Synonyms	RAF1; v-raf-1 murine leukemia viral oncogene homolog 1; RAF proto-oncogene serine/threonine-protein kinase; c Raf; CRAF; Raf 1; Oncogene RAF1; proto-oncogene c-RAF; raf proto-oncogene serine/threonine protein kinase; NS5; Raf-1; c-Raf;
GeneID	5894
Uni ProtID	P04049
mRNA Refseq	BC018119
Chromosome Location	3p25
Function	ATP binding; MAP kinase kinase kinase activity; Ras GTPase binding; metal ion binding; mitogen-activated protein kinase kinase binding; nucleotide binding; protein binding; protein heterodimerization activity; protein kinase acti
Pathway	ARMS-mediated activation, organism-specific biosystem; Activation of NMDA receptor upon glutamate binding and postsynaptic events, organism-specific biosystem; Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; Adaptive Immune System, organism-specific biosystem; Androgen Receptor Signaling Pathway, organism-specific biosystem; Axon guidance, organism-specific biosystem;
MIM	164760

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Anlotinib is an effective drug for treating advanced non-small cell lung cancer (NSCLC), but resistance often develops during treatment. RAF1, a serine/threonine kinase involved in cancer progression, has limited research in NSCLC, particularly regarding anlotinib resistance. Here, bioinformatics analysis showed low RAF1 expression levels in lung cancer tissues in the TCGA and GEPIA databases. Further pathway analysis revealed a positive correlation between RAF1 expression and targeted therapy resistance, and a negative correlation with the expression of the anti-apoptotic protein Bcl-2. Immunohistochemical analysis showed that high RAF1 expression in NSCLC tissues was associated with anlotinib resistance. In vitro experiments demonstrated that RAF1 is involved in anlotinib resistance in NSCLC cells. Overexpression of RAF1 increased the viability of PC9 and PC9/AR cells and reduced apoptosis, while knockdown of RAF1 produced the opposite effect. Therefore, these results suggest that RAF1 mediates anlotinib resistance in NSCLC cells by regulating apoptosis and may serve as a predictive biomarker for anlotinib resistance in patients with advanced lung cancer.

To investigate the potential function of RAF1 in non-small cell lung cancer (NSCLC) cells, researchers constructed RAF1-overexpressing and RAF1-knockdown cells. CCK-8 assays showed that RAF1 overexpression significantly improved the survival rate of PC9 and PC9/AR cells compared to the control/pc-NC group (Figure 1A1), while RAF1 knockdown exhibited the opposite effect (Figure 1A2). Flow cytometry analysis revealed that RAF1-overexpressing cells had a decreased apoptosis rate (Figure 1B1, C1), while RAF1-knockdown cells had an increased apoptosis rate (Figure 1B2, C2). Western blot analysis showed that RAF1 overexpression reduced Bax expression in PC9 and PC9/AR cells and significantly increased Bcl-2 expression (Figure 1D1, E1). Conversely, RAF1-knockdown cells showed upregulated Bax expression and inhibited Bcl-2 expression (Figure 1D2, E2). These observations suggest that RAF1 regulates the viability and apoptosis of PC9 and PC9/AR cells.

Figure 1. Effects of RAF1 overexpression and knockdown on PC9 and PC9/AR cells viability and apoptosis. (Wu S, et al., 2025)

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