This product offers a CRISPR/Cas9-edited polyclonal knockout cell population targeting the KDM5B gene in HGC-27 human gastric carcinoma cells. The polyclonal format provides a heterogeneous loss-of-function model, avoiding clonal bias and enabling robust investigation of KDM5B??s epigenetic regulatory functions in cancer.
The HGC-27 cell line, derived from lymph node metastasis of gastric adenocarcinoma, is an adherent epithelial model of metastatic gastric cancer. Its Homo sapiens origin and retention of key oncogenic pathways make it suitable for studying molecular mechanisms of tumor dissemination and therapeutic resistance.
KDM5B functions as a histone demethylase that specifically erases H3K4me2/3 marks, acting as a transcriptional repressor. It is regulated by upstream signals including MYC, HIF1A, and E2F transcription factors, with negative post-transcriptional control by miR-137 and miR-29c. KDM5B forms complexes with HDAC1/2, SIN3A, and PRC2 subunits EZH2/SUZ12, and it physically interacts with REST, NANOG, and MYC. At promoters of key targets such as CDKN1A (p21), BAX, and HOXA cluster genes, it demethylates H3K4me3, repressing their expression to drive cell cycle progression and block apoptosis. Disruption of KDM5B by CRISPR/Cas9 lifts this repression, upregulating p21 and BAX to induce cell cycle arrest and apoptosis, while also dampening PI3K/AKT, Wnt/??-catenin, and p53 signaling pathways.
In gastric adenocarcinoma, KDM5B overexpression drives stemness, metastasis, and drug resistance by epigenetically silencing tumor suppressors. The HGC-27 knockout model thus permits dissection of KDM5B??s role in gastric cancer cell proliferation, migration, and epithelial-mesenchymal transition. It is ideal for probing crosstalk between histone methylation dynamics and oncogenic pathways such as p53, PI3K/AKT, and Wnt/??-catenin, which modulate downstream effectors like Cyclin D1 and ??-catenin.
This knockout cell population supports a broad array of assays, including Western blotting, RT-qPCR, ChIP-qPCR, cell proliferation and colony formation, migration and invasion, apoptosis and cell cycle analysis, RNA-seq, and drug sensitivity profiling. Applications range from target validation for epigenetic inhibitors and differentiation therapy agents to mechanistic studies of gastric cancer stemness and metastasis. It is also well-suited for high-throughput functional genomics screens to uncover synthetic lethal partners. For further technical details, please contact Ascent Research.
