The ANLN Knockout HGC-27 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma cell line, engineered for targeted disruption of the ANLN gene. This loss-of-function model is supplied as a heterogeneous polyclonal pool, enabling robust and reproducible assessment of ANLN-dependent phenotypes without single-cell cloning artifacts. The polyclonal format captures clonal diversity, which may better reflect tumor heterogeneity in experimental settings. As a ready-to-use cellular tool, it is optimized for downstream functional assays, including proliferation, migration, and signaling studies, and is suitable for both short-term and stable long-term experiments.
HGC-27 is an adherent epithelial cell line originally isolated from the lymph node metastasis of a patient with gastric adenocarcinoma. This cell line retains key characteristics of metastatic gastric cancer, including invasive capacity, altered cell cycle regulation, and responsiveness to chemotherapeutic agents. HGC-27 cells harbor molecular features relevant to advanced disease, such as dysregulated PI3K/AKT signaling and E-cadherin-mediated adhesion changes, making them an established model for studying tumor progression, metastasis, and drug resistance mechanisms. The gastric carcinoma origin and metastatic background offer a clinically relevant context for investigating ANLN function in aggressive cancer phenotypes.
ANLN encodes anillin, an evolutionarily conserved actin-binding protein essential for cytokinesis and actomyosin contractility. It is activated downstream of RhoA-GTP and regulated by Rho guanine nucleotide exchange factors such as ECT2, and its expression is modulated by transcription factors including FOXM1 and microRNAs such as miR-218. ANLN directly interacts with F-actin, myosin II, septins, and E-cadherin?Ccatenin complexes, positioning it at the interface between the cytoskeleton and cell adhesion. It promotes actin polymerization through RhoA?CROCK?CLIMK?Ccofilin signaling and participates in feedback regulation of RhoA. In dividing cells, ANLN coordinates the contractile ring assembly and ingression, while in interphase, it influences cell?Ccell junctions and cortical tension, thereby linking cell division to motility.
In HGC-27 gastric cancer cells, ANLN is frequently overexpressed and associated with poor prognosis, enhanced proliferation, and metastatic behavior. CRISPR/Cas9-mediated disruption of ANLN in this cell line is expected to impair cytokinesis, leading to multinucleation and cell cycle arrest, while also attenuating actomyosin contractility and RhoA-driven invasion. The resultant defects in actin cytoskeleton dynamics and E-cadherin?Cmediated adhesion may reduce transwell migration and wound healing capacity. Because HGC-27 cells exhibit constitutive activation of survival pathways such as PI3K/AKT, ANLN knockout may also sensitize cells to apoptosis or overcome chemoresistance, providing a physiologically relevant model to dissect molecular drivers of gastric cancer aggressiveness.
This ANLN polyclonal knockout cell model supports diverse research applications, including the study of cytokinesis failure and its consequences on genome instability, dissection of Rho GTPase signaling in 3D invasion assays, and evaluation of drug response alterations in the context of actin cytoskeleton disruption. Representative experimental approaches include cell viability and apoptosis assays, cell cycle analysis by flow cytometry, wound healing and transwell invasion assays, immunofluorescence staining for F-actin and anillin localization, and western blotting for phospho-RhoA and E-cadherin. The system is also suitable for co-culture or tumor microenvironment studies to investigate how ANLN loss influences tumor?Cstroma interactions. For detailed product information or customized applications, please contact Ascent Research.
