The KDM5D Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population, generated from the HGC-27 human gastric carcinoma cell line to disrupt KDM5D expression. As a polyclonal pool, this product offers a heterogeneous mix of edited alleles, avoiding clonal selection artifacts and providing a reliable loss-of-function system for investigating KDM5D-dependent pathways in gastric cancer research.
The HGC-27 cell line is a well-characterized model of human gastric adenocarcinoma, originally established from the lymph node metastasis of a gastric cancer patient. These cells exhibit an epithelial-like morphology and retain key molecular features of gastric carcinoma, including active signaling pathways relevant to tumor progression and metastasis. As a gastric cancer cell line, HGC-27 is widely used for studying mechanisms of invasion, migration, and epithelial-mesenchymal transition (EMT), making it an appropriate host for KDM5D knockout studies.
KDM5D encodes a histone lysine demethylase that specifically removes methyl groups from di- and monomethylated lysine 4 on histone H3 (H3K4me2/me1), acting as a transcriptional repressor. It is a Y chromosome-linked gene subject to regulation by androgen receptor signaling and Y chromosome dosage. KDM5D participates in chromatin remodeling complexes and interacts with corepressors such as HDAC1/2, the androgen receptor, and the REST corepressor complex. Its demethylase activity primarily targets promoter regions of genes involved in EMT, including CDH1 (encoding E-cadherin), VIM (vimentin), ZEB1, and SNAI1, thereby repressing their transcription and promoting an epithelial phenotype.
In the HGC-27 gastric carcinoma background, knockout of KDM5D disrupts this repressive mechanism, leading to increased H3K4 methylation at its target loci and derepression of mesenchymal gene expression. This shift activates the EMT program, enhancing cell motility, invasiveness, and metastatic potential. Consequently, the KDM5D Knockout HGC-27 polyclonal cells serve as a physiologically relevant model to dissect the epigenetic control of EMT in gastric cancer and to explore the tumor-suppressive role of the Y chromosome in epithelial malignancies.
These polyclonal knockout cells are suitable for a broad range of functional studies. Researchers can employ Western blotting, RT-qPCR, and immunofluorescence to quantify changes in EMT markers, while ChIP-qPCR enables analysis of H3K4 methylation at target promoters. Migration and invasion assays (e.g., Transwell) provide direct readouts of metastatic behavior. RNA-seq transcriptome profiling can reveal global gene expression changes, and the model is amenable to testing epigenetic inhibitors targeting KDM5D or its interactors. Key applications include functional studies of KDM5D in gastric cancer metastasis, epigenetic regulation of EMT, Y chromosome gene function in cancer, and validation of epigenetic drug targets. For further details, please contact Ascent Research.
