The HCFC1R1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population specifically designed for loss-of-function analysis of the HCFC1R1 gene (also known as HPIP) in a human gastric adenocarcinoma model. This product comprises a heterogeneous pool of HGC-27 cells in which the HCFC1R1 locus has been disrupted by CRISPR/Cas9-mediated gene editing, allowing researchers to assess gene function at the population level without the confounding effects of clonal selection. The polyclonal format is particularly advantageous for studies requiring representation of diverse knockout genotypes, such as functional genomics screens and downstream phenotypic assays including proliferation, migration, and transcriptional reporter analyses.
HGC-27 is a poorly differentiated gastric adenocarcinoma epithelial cell line originally established from a lymph node metastasis of a signet ring cell gastric carcinoma. These cells display an adherent epithelial morphology and are widely utilized as an in vitro model for metastatic gastric cancer research. The HGC-27 line retains hallmark features of aggressive gastric malignancy, including high proliferative rate and invasive capacity, making it a clinically relevant host for investigating the molecular drivers of gastric cancer progression and metastasis.
HCFC1R1 functions as a scaffold protein that bridges HCFC1 and PBX1 transcription factors, markedly enhancing their transcriptional regulatory activity. It integrates signals from Wnt, TGF-??, and growth factor pathways, acting as a key node in oncogenic signaling. Upstream, its expression is induced by growth factors such as EGF and HGF, as well as by Wnt ligands and TGF-??. HCFC1R1 forms multiprotein complexes with ??-catenin, CBP/p300, HCFC1, and PBX1, and it drives the transcription of downstream targets including MMP9, Cyclin D1, c-Myc, and CD44, thereby promoting cell cycle progression, migration, and invasion.
In the HGC-27 gastric cancer cell context, HCFC1R1 is a well-established driver of proliferation, migration, and invasion. Disruption of HCFC1R1 expression via CRISPR/Cas9 polyclonal knockout in these cells leads to attenuated activation of the HCFC1-PBX1 transcriptional complex and a corresponding reduction in target gene expression, thereby impairing the cells?? malignant properties. Consequently, this knockout model provides a powerful platform for dissecting the precise role of HCFC1R1 in metastatic gastric cancer and for evaluating how its scaffolding function contributes to signaling network rewiring in poorly differentiated gastric tumors.
This polyclonal knockout model is well-suited for mechanistic studies of gastric cancer metastasis, high-throughput screening of compounds targeting the HCFC1-PBX1 transcriptional axis, and detailed functional interrogation of Wnt and TGF-?? signaling in gastric cancer. Typical assays used with these cells include western blotting, RT-qPCR, MTT/CCK-8 proliferation assays, Transwell migration and invasion assays, co-immunoprecipitation, and luciferase reporter assays. For additional technical details or ordering information, contact Ascent Research.
