Panoply™ Human MUC1 Knockdown Stable Cell Line

Name: Panoply™ Human MUC1 Knockdown Stable Cell Line
SKU: CSC-DC009927
Availability: InStock

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

Cat. No. : CSC-DC009927

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

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Gene Information

Cat. No.	CSC-DC009927
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	MUC1
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	MUC1 mucin 1, cell surface associated [ Homo sapiens ]
Gene Symbol	MUC1
Synonyms	MUC1; mucin 1, cell surface associated; mucin 1, transmembrane , PUM; mucin-1; CD227; PEM; episialin; DF3 antigen; H23 antigen; krebs von den Lungen-6; mucin 1, transmembrane; tumor-associated mucin; carcinoma-associated mucin; polymorphic epithelial mucin; peanut-reactive urinary mucin; tumor associated epithelial mucin; breast carcinoma-associated antigen DF3; tumor-associated epithelial membrane antigen; EMA; PUM; KL-6; MAM6; PEMT; H23AG; MUC-1; MUC-1/X; MUC1/ZD; MUC-1/SEC;
Gene ID	4582
Uni Prot ID	P15941
m RNA Refseq	BC120975
Chromosome Location	1q22
Function	RNA polymerase II core promoter proximal region sequence-specific
Pathway	IL-7 Signaling Pathway, organism-specific biosystem; Metabolism of proteins, organism-specific biosystem; O-linked glycosylation of mucins, organism-specific biosystem; Post-translational protein modification, organism-specific biosystem; T Cell Receptor Signaling Pathway, organism-specific biosystem; Termination of O-glycan biosynthesis, organism-specific biosystem;
MIM	158340

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Mucin 1 (MUC1) is a transmembrane glycoprotein involved in the development and progression of various cancers. However, the role of MUC1 in glioblastoma (GBM) remains unclear. Here, researchers investigated the anti-cancer mechanism of MUC1 inhibition in GBM. MUC1 expression levels were analyzed in human glioma and matched normal brain tissue. Results showed that MUC1 was overexpressed in GBM and negatively correlated with overall survival. Furthermore, MUC1 gene knockdown was performed to investigate its effects in GBM cell lines. Results showed that MUC1 knockdown inhibited cell proliferation and caused cell cycle arrest in the G1 phase. MUC1 knockdown decreased RB1 phosphorylation and increased CDKN1B expression. Gene set enrichment analysis revealed that a series of genes related to cell cycle, telomere maintenance, and transforming growth factor β (TGF-β) signaling during epithelial-mesenchymal transition (EMT) were affected by MUC1 knockdown. Notably, knockdown of MUC1 reduced TERT expression, impaired telomerase activity, and shifted the telomere maintenance mechanism to alternative telomere lengthening (ALT). These findings support the role of MUC1 in glioblastoma (GBM) tumor progression and suggest that MUC1 could be a therapeutic target for cell cycle regulation and telomere maintenance mechanisms.

To investigate the potential mechanism underlying the decreased cell viability caused by MUC1 knockdown, the researchers performed cell cycle analysis. Flow cytometry revealed that after MUC1 knockdown, the cell cycle arrested at the G0/G1 phase (Figures 1A and B). Among G1 phase cell cycle regulators, CDKN1B protein expression was upregulated, while phosphorylation of retinoblastoma 1 (RB1) was decreased after MUC1 knockdown (Figure 1C). Control and MUC1 knockdown cells were stained with Annexin V and 7-AAD to investigate whether G1 phase cell cycle arrest was associated with apoptosis. However, there was no statistically significant difference in apoptosis rates between control and MUC1 knockdown cells.

Figure 1. MUC1 knockdown attenuates cell cycle progression at G1 phase. (Kim S, et al., 2020)

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