The DYNLT1 Knockout HGC-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal cell population derived from the HGC-27 human gastric adenocarcinoma cell line, featuring targeted disruption of the DYNLT1 gene. This loss-of-function model enables investigation of DYNLT1-dependent processes without altering the polyclonal background, providing a heterogeneous knockout system suitable for functional genomics studies in a gastric cancer context.
HGC-27 is a well-characterized human gastric adenocarcinoma cell line originally established from a metastatic lymph node. Its metastatic origin and adherent epithelial morphology make it an appropriate model for dissecting molecular mechanisms of gastric cancer progression and metastasis. In this polyclonal knockout pool, DYNLT1 ablation is introduced into a cell background that retains native gastric cancer signaling networks, offering a biologically relevant platform for mechanistic studies.
DYNLT1 encodes a subunit of the cytoplasmic dynein motor complex, which mediates minus-end-directed transport along microtubules. It interacts with key dynein components including dynein intermediate chain, dynactin subunit p150(Glued) (DCTN1), and dynein light chain LC8 (DYNLL1). DYNLT1 is regulated by cell cycle regulators and stress signaling pathways and functions downstream of these cues to modulate cargo trafficking. Critically, DYNLT1 participates in mitotic spindle organization through interactions with mitotic checkpoint proteins, and it directly associates with the pro-apoptotic factor BCL2L11 (BIM), linking dynein function to apoptotic signaling. Additionally, DYNLT1 interacts with viral proteins such as HPV E6 and HIV-1 Vif, underscoring its role in diverse cellular pathways.
In the HGC-27 background, disruption of DYNLT1 expression impairs dynein-mediated retrograde transport, potentially altering the intracellular distribution of organelles and signaling molecules. Given DYNLT1??s involvement in mitotic spindle assembly and BCL2L11-mediated apoptosis, knockout cells may display defects in chromosome segregation, mitotic checkpoint control, and apoptotic sensitivity. These perturbations are expected to influence gastric cancer cell proliferation, survival, and invasive behavior, making this model valuable for studying the contributions of dynein-dependent transport to oncogenic processes and metastatic dissemination.
This polyclonal knockout cell pool is suited for a range of advanced applications, including gastric cancer research, intracellular transport studies, mitotic spindle assembly analysis, apoptotic signaling investigation, and drug target validation. Typical assays include western blotting, co-immunoprecipitation, immunofluorescence, MTT proliferation assays, Annexin V apoptosis assays, migration assays, live-cell imaging of organelle movement, and mitotic checkpoint analyses. For further technical details, please contact Ascent Research.
