In Stock Cell Lines
Homo sapiens (Human)
Stomach
Adherent
The BCL2 Knockout HGC-27 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from HGC-27 human gastric adenocarcinoma cells. This model disrupts the BCL2 gene, removing anti-apoptotic regulation and sensitizing cells to intrinsic apoptosis through mitochondrial outer membrane permeabilization and cytochrome c release. The HGC-27 background provides a poorly differentiated, metastatic gastric cancer platform for studying apoptosis mechanisms, drug resistance, and cell death signaling. Key readouts include changes in BAX, caspase-3 cleavage, and mitochondrial membrane potential. This tool supports applications such as Western blotting, flow cytometry, and co-immunoprecipitation to investigate BCL2 family interactions.
ISG20 Knockout HAP1 Polyclonal Cells
Cat. No. ARG22854
ACO1 Knockout huh-7 Polyclonal Cells
Cat. No. ARG27778
HLA-DRA Knockout CaSki Polyclonal Cells
Cat. No. ARG35475
ID3 Knockout A549 Polyclonal Cells
Cat. No. ARG35621
CALHM2 Knockout SKOV3 Polyclonal Cells
Cat. No. ARG41861
MAPK7 Knockout CaSki Polyclonal Cells
Cat. No. ARG9789
The BCL2 Knockout HGC-27 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the HGC-27 human gastric adenocarcinoma cell line. This cell line features targeted disruption of the BCL2 gene, leading to loss of BCL2 protein expression and function. The knockout model provides a defined system for studying apoptosis regulation, drug resistance, and cell survival mechanisms in a gastric cancer context. The product is supplied as a validated knockout cell line ready for downstream assays including Western blotting, flow cytometry, and cell viability analyses.
HGC-27 is a poorly differentiated gastric adenocarcinoma cell line established from lymph node metastasis of a human male patient. The poorly differentiated phenotype reflects aggressive tumor behavior with invasive and metastatic capacity, making it a relevant model for advanced gastric cancer research. HGC-27 cells retain molecular features of gastric adenocarcinoma, including epithelial-mesenchymal transition traits, and serve as a platform to investigate oncogenic signaling and therapeutic vulnerabilities in this malignancy.
BCL2 is an anti-apoptotic regulator that inhibits mitochondrial outer membrane permeabilization (MOMP) by binding and neutralizing pro-apoptotic effectors such as BAX and BAK. BCL2 is regulated by upstream signals including NF-??B, STAT3, and PI3K-AKT, and is induced by cytokines like IL-3 and IL-6. Upon loss of BCL2, pro-apoptotic BIM and BID are freed to activate BAX and BAK, causing cytochrome c release and subsequent activation of caspase-9 and caspase-3. BCL2 also interacts with mitochondrial components VDAC and PP1. Disruption of BCL2 in this knockout line removes anti-apoptotic protection, sensitizing cells to intrinsic apoptosis.
In the HGC-27 gastric adenocarcinoma background, BCL2 knockout abolishes anti-apoptotic signaling and enhances susceptibility to apoptosis induced by chemotherapeutic stress or growth factor deprivation. This sensitization is critical for modeling drug resistance mechanisms, as BCL2 upregulation often underlies therapeutic failure in gastric cancers. The knockout line allows mechanistic dissection of BCL2-dependent survival pathways and evaluation of compensatory responses from other BCL2 family members in poorly differentiated, metastatic cancer cells.
Researchers can employ this knockout line for apoptosis mechanism studies and drug resistance research. Representative assays include Western blotting for BCL2, BAX, and cleaved caspase-3; flow cytometry with Annexin V/PI; caspase activity assays; cell viability MTT assays under stress; co-immunoprecipitation of BCL2 family complexes; and mitochondrial membrane potential measurement using JC-1. These tools facilitate investigation of cell death signaling and gastric cancer progression. For further information, please contact Ascent Research.
