The CD109 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the HGC-27 gastric carcinoma cell line. This product constitutes a heterogeneous pool of alleles bearing disruptions at the CD109 locus, yielding a loss-of-function model that avoids the clonal biases inherent in single-cell-derived lines. The polyclonal format preserves the complexity of the knockout across many individual edits, making it well-suited for pooled functional analyses and experiments where representation of genetic diversity is critical. The CRISPR/Cas9-mediated gene disruption targets CD109 expression, enabling researchers to study the biological consequences of CD109 ablation in a relevant cancer model.
HGC-27 is a human gastric cancer cell line originally isolated from a lymph node metastasis of a gastric carcinoma, widely employed as a model for gastric adenocarcinoma. These cells exhibit hallmark features of gastric tumorigenesis, including dysregulated survival signaling, migratory capacity, and invasive potential. The HGC-27 background provides a clinically pertinent host line in which CD109 is endogenously expressed, allowing the investigation of CD109 function within the native genomic and signaling context of an aggressive gastric cancer.
CD109 encodes a glycosylphosphatidylinositol (GPI)-anchored cell surface antigen that functions as a critical negative regulator of the transforming growth factor-beta (TGF-??) pathway. Mechanistically, CD109 binds to the TGF-?? receptors TGFBR1 and TGFBR2, facilitating their internalization and subsequent degradation in a process that involves the adaptor proteins SMAD7 and the E3 ubiquitin ligase SMURF2. Upstream TGF-?? ligands TGFB1, TGFB2, and TGFB3 activate the canonical receptor complex, and CD109 dampens this signal by reducing receptor availability. Disruption of CD109 is therefore expected to relieve this suppressive brake, leading to enhanced receptor stability and increased phosphorylation of the downstream effectors SMAD2 and SMAD3. The activated SMAD2/3 proteins complex with SMAD4 and translocate to the nucleus, where they drive the transcription of target genes such as SERPINE1, COL1A1, SNAI1, and VIM, which are involved in extracellular matrix remodeling and epithelial-mesenchymal transition.
In the HGC-27 gastric cancer model, CD109 knockout provides a powerful tool to elucidate how TGF-?? signaling dynamics influence tumor behavior. CD109 is frequently overexpressed in gastric carcinomas and has been associated with immune evasion, aggressive tumor growth, and poor prognosis. By eliminating CD109 expression, this polyclonal knockout population permits systematic interrogation of the reciprocal relationship between CD109-driven receptor turnover and the output of the TGF-??, JAK-STAT, and PI3K-AKT pathways. The model can be used to assess how enhanced TGF-?? signaling affects HGC-27 cell proliferation, migration, and invasion, offering insights into the molecular determinants of gastric cancer metastasis.
Typical research applications include western blotting for SMAD2/3 phosphorylation in response to TGF-?? stimulation, RT-qPCR analysis of transcriptional targets (e.g., SERPINE1, COL1A1, SNAI1, VIM), and functional assays such as migration, invasion, and cell viability to measure phenotypic consequences. Co-immunoprecipitation experiments can quantify altered interactions between CD109, TGFBR1, and TGFBR2, while immunofluorescence microscopy confirms loss of CD109 localization. This polyclonal knockout population is also amenable to drug screening studies targeting the TGF-?? signaling axis or compensatory pathways. For additional product specifications and experimental protocols, please contact Ascent Research.
