The DYNC1LI1 Knockout HGC-27 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal cell population derived from the human HGC-27 gastric adenocarcinoma cell line, designed to disrupt the endogenous DYNC1LI1 locus. This loss-of-function model enables investigation of cytoplasmic dynein 1 light intermediate chain function in a poorly differentiated epithelial gastric cancer background. The polyclonal format ensures diverse mutational outcomes across the cell population, providing a robust system for functional studies without the clonal selection biases inherent to monoclonal lines.
HGC-27 is a well-characterized human gastric adenocarcinoma cell line isolated from a poorly differentiated tumor. As an epithelial cell type, HGC-27 retains features relevant to gastric cancer biology, including active intracellular trafficking, migratory capacity, and proliferative signaling networks. This cell line is extensively used in cancer research to study mechanisms of tumor progression, metastasis, and therapeutic response.
DYNC1LI1 encodes the light intermediate chain 1 of cytoplasmic dynein, a major minus-end-directed microtubule motor complex. The protein interacts directly with the dynein heavy chain (DYNC1H1) and multiple dynactin subunits (e.g., DCTN1, DCTN2), as well as with regulatory cofactors including NDE1, NDEL1, and LIS1 (PAFAH1B1). DYNC1LI1 is critical for dynein complex stability and cargo recruitment, mediating retrograde transport of organelles such as lysosomes and endosomes, mitotic spindle orientation, and cell migration. Upstream regulation involves CDK1-mediated phosphorylation and dynactin-dependent activation, while downstream effects include positioning of lysosomes and orientation of the mitotic spindle. Thus, DYNC1LI1 serves as a key nodal point linking dynein motor activity to diverse cellular outputs.
In the HGC-27 gastric cancer context, disruption of DYNC1LI1 impairs cytoplasmic dynein-dependent trafficking and mitotic functions, potentially compromising lysosomal positioning, autophagy flux, and directional cell migration. Given the established roles of dynein in cancer cell invasion and metastasis, this knockout model offers a relevant platform to dissect how dynein light intermediate chain dysfunction affects gastric adenocarcinoma cell behavior. The polyclonal knockout population also facilitates study of heterogeneous loss-of-function effects within a tumor-relevant background.
This product is suited for a range of research applications, including examination of dynein-mediated organelle transport via live-cell imaging, assessment of lysosomal trafficking by immunofluorescence, and analysis of mitotic spindle orientation using fixed-cell assays. Additionally, it enables functional studies of cell migration and invasion, co-immunoprecipitation of dynein-dynactin components, and investigation of autophagy in cancer cells. The DYNC1LI1 Knockout HGC-27 Polyclonal Cells provide a versatile tool for exploring the roles of cytoplasmic dynein in gastric cancer and related neurodevelopmental disorder mechanisms. For further information, please contact Ascent Research.
