Panoply™ Human HDAC2 Over-expressing Stable Cell Line

Name: Panoply™ Human HDAC2 Over-expressing Stable Cell Line
SKU: CSC-SC006887
Availability: InStock

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

Cat. No. : CSC-SC006887

Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x10⁶ frozen cells/vial

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Cell Line Information

Cell Culture Information

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Gene Information

Cat. No.	CSC-SC006887
Description	Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level.
Target Gene	HDAC2
Gene Species	Homo sapiens (Human)
Host Cell	HEK293 (CHO and other cell types are also available)
Host Cell Species	Species varies
Applications	1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research
Size	2 × 10^6 cells / vial
Stability	Validated for at least 10 passages
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid nitrogen
Shipping	Dry Ice

Revival

Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media.

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	HDAC2 histone deacetylase 2 [ Homo sapiens ]
Gene Symbol	HDAC2
Synonyms	HD2; RPD3; YAF1
GeneID	3066
Uni ProtID	Q92769
mRNA Refseq	NM_001527.3
Protein Refseq	NP_001518.3
Chromosome Location	6q21
Function	NAD-dependent histone deacetylase activity (H3-K14 specific); NAD-dependent histone deacetylase activity (H3-K18 specific); NAD-dependent histone deacetylase activity (H3-K9 specific); NAD-dependent histone deacetylase activity (H4-K16 specific); chromatin binding; enzyme binding; histone deacetylase activity; protein binding; protein deacetylase activity; sequence-specific DNA binding; transcription factor binding;
Pathway	Alcoholism, organism-specific biosystem; Alcoholism, conserved biosystem; Cell cycle, organism-specific biosystem; Cell cycle, organism-specific biosystem; Cell cycle, conserved biosystem; Chronic myeloid leukemia, organism-specific biosystem; Chronic myeloid leukemia, conserved biosystem;
MIM	605164

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Invasion and metastasis are the main causes of death in patients with malignant tumors, including gastric cancer. Here, researchers investigated the effects of methionine restriction (MR) on gastric cancer metastasis and its underlying mechanisms. The results showed that MR inhibited the migration, invasion, and lung metastasis of gastric cancer cells. MR increased E-cadherin expression while decreasing H3K27me3 levels in the E-cadherin promoter region. E-cadherin expression in gastric cancer cells was negatively regulated by HDAC2. Overexpression of HDAC2 decreased H3K27Ac levels in the E-cadherin promoter region, while knockdown of HDAC2 increased H3K27Ac levels. Under MR conditions, knockdown of HDAC2 further upregulated E-cadherin expression and inhibited the migration, invasion, and lung metastasis of gastric cancer cells. MR combined with HDAC2 knockdown promoted E-cadherin expression by mediating its methylation and acetylation, thereby inhibiting the invasion, migration, and lung metastasis of gastric cancer cells. These studies provide a new theoretical basis for the inhibitory effect of MR on gastric cancer.

Considering the elevated expression of HDAC2 in gastric cancer and its regulatory role in E-cadherin histone deacetylation, researchers investigated the regulatory effect of HDAC2 on E-cadherin in gastric cancer cells. They constructed HDAC2-overexpressing MKN45 and AGS cells and HDAC2-knockdown MKN45 and AGS cells. qRT-PCR and Western blot analysis showed that E-cadherin expression was suppressed in HDAC2-overexpressing MKN45 and AGS cells, while E-cadherin expression increased in HDAC2-knockdown cells (Figure 1A-C). The researchers also examined apoptosis after HDAC2 knockdown, and the results showed that HDAC2 knockdown did not significantly affect apoptosis in gastric cancer cells. Chromatin immunoprecipitation (ChIP) experiments were performed to confirm that HDAC2 regulates the acetylation of the E-cadherin promoter, using an H3K27ac antibody for immunoprecipitation. The results showed that H3K27ac levels in the E-cadherin promoter region were decreased in HDAC2-overexpressing cells, while H3K27ac levels in the E-cadherin promoter region were increased in HDAC2-knockdown cells (Figure 1D). These data suggest that HDAC2 may inhibit E-cadherin transcription by suppressing the acetylation of the E-cadherin promoter.

Figure 1. The regulatory effect of HDAC2 on the acetylation of the E-cadherin promoter. (Li Y, et al., 2023)

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