The CASP6 Knockout HGC-27 Polyclonal Cells consist of a CRISPR/Cas9-mediated polyclonal knockout cell population targeting the CASP6 gene in the HGC-27 human gastric adenocarcinoma cell line. This format delivers a heterogeneous loss-of-function model that retains native genetic diversity, allowing researchers to assess the collective impact of CASP6 disruption without clonal bias. It is particularly suited for studying dynamic biological processes where cellular heterogeneity is physiologically relevant.
HGC-27 is a human gastric carcinoma cell line derived from a lymph node metastasis of a poorly differentiated adenocarcinoma. Exhibiting epithelial morphology, it is extensively used in gastric cancer research to examine tumor cell proliferation, metastasis, and drug resistance. The cell line expresses characteristic markers of gastric epithelium and has been employed in numerous studies elucidating signaling pathways driving gastric carcinogenesis, making it an ideal host for investigating genes implicated in aggressive cancer phenotypes and therapeutic vulnerabilities.
CASP6 encodes an executioner caspase that functions downstream of initiator caspases CASP8 and CASP9 in both intrinsic and extrinsic apoptotic pathways. Upon activation, CASP6 proteolytically cleaves lamin A/C (LMNA), PARP1, and ICAD, leading to nuclear disassembly and cell death. Upstream regulation involves p53 and RSK2 phosphorylation, while interacting partners include CASP3, CASP7, XIAP, and SMAC/DIABLO. In addition to apoptosis, CASP6 contributes to neurodegeneration by cleaving tau and amyloid precursor protein (APP), connecting it to Alzheimer disease and neurotrophin signaling pathways.
In the context of gastric cancer, Caspase-6 dysfunction is associated with apoptosis evasion and chemoresistance, particularly in poorly differentiated tumors like HGC-27. The knockout of CASP6 in this cell line permits dissection of its tumor-suppressive or oncogenic contributions, including potential involvement in cell differentiation and inflammatory processes. This model is invaluable for probing how loss of CASP6 modifies sensitivity to standard chemotherapies such as cisplatin and for identifying downstream mediators of drug response, while also providing a platform to study non-apoptotic roles in tumor invasion and signaling crosstalk.
Researchers can apply these polyclonal knockout cells to a variety of assays. Apoptosis evaluation via Annexin V/PI staining and Caspase-6 activity assays quantifies programmed cell death defects. Western blotting for cleaved substrates confirms functional knockout, while MTT viability and cisplatin sensitivity assays assess chemotherapeutic response. Transwell migration/invasion assays measure metastatic potential, and co-immunoprecipitation reveals altered protein interactions. RNA-seq transcriptomic profiling captures global gene expression changes. For further details or technical support, please contact Ascent Research.
