Panoply™ Human MYD88 Knockdown Stable Cell Line

Name: Panoply™ Human MYD88 Knockdown Stable Cell Line
SKU: CSC-DC009978
Availability: InStock

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

Cat. No. : CSC-DC009978

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-DC009978
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	MYD88
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	MYD88 myeloid differentiation primary response gene (88) [ Homo sapiens ]
Gene Symbol	MYD88
Synonyms	MYD88D
GeneID	4615
Uni ProtID	Q99836
mRNA Refseq	NM_001172566.1
Protein Refseq	NP_001166037.1
Chromosome Location	3p22
Function	TIR domain binding; Toll binding; death receptor binding; identical protein binding; protein binding;
Pathway	Activated TLR4 signalling, organism-specific biosystem; African trypanosomiasis, organism-specific biosystem; African trypanosomiasis, conserved biosystem; Apoptosis, organism-specific biosystem; Apoptosis, conserved biosystem; Apoptosis Modulation and Signaling, organism-specific biosystem; Chagas disease (American trypanosomiasis), organism-specific biosystem;
MIM	602170

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The role of myeloid differentiation factor 88 (MyD88) in malignant tumors remains unclear. In this study, researchers investigated the function and underlying mechanisms of MyD88 in colorectal cancer using SW480 and HCT116 cell lines (in vitro) and a nude mouse model (in vivo). In vitro experiments demonstrated that silencing MyD88 in SW480 and HCT116 cells significantly inhibited cell growth and invasion. Furthermore, MyD88 knockdown modulated the MyD88-NF-κB/AP-1 signaling pathway in these cells. In vivo experiments showed that MyD88 knockdown suppressed tumor growth in a subcutaneous xenograft model using HCT116 cells. The study revealed that silencing the MyD88 gene affected the proliferation, invasion, and migration capabilities of colorectal cancer cells. Further validation confirmed that MyD88 knockdown reduced the activity of the NF-κB and AP-1 pathways. These results indicate that MyD88 plays a crucial role in promoting the progression of colorectal cancer and holds promise as a potential biomarker for its diagnosis and prognosis.

To evaluate the inhibitory effect of MyD88 knockdown on cell migration in colorectal cancer cells, researchers assessed the migratory capacity of SW480 and HCT116 cells following MyD88 knockdown using Transwell and wound-healing assays. Similarly, Transwell assays were employed to evaluate the invasive capacity of SW480 and HCT116 cells. Changes in cell migration were confirmed by observing the extent of wound closure in the wound-healing assay. The results showed that the rate of wound closure in MyD88-knockdown SW480 and HCT116 cells was lower than that in the control group. To further validate the migration assay findings, Transwell assays were conducted. The results demonstrated that the number of colorectal cancer cells migrating through the Transwell polycarbonate membrane was significantly lower in the MyD88-knockdown SW480 and HCT116 cells compared to the control group (Figures 1A and B). These results indicate that MyD88 knockdown significantly inhibited cell migration compared to the negative control (NC) group. In vitro invasion assays revealed that the number of cells penetrating the basement membrane was significantly lower in MyD88-knockdown SW480 and HCT116 cells than in the control group (Figures 1C and D).

Figure 1. Effects of siMyD88 on SW480 and HCT116 cells migration and invasion. (Zhu G, et al., 2020)

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