The HDAC6 Knockout HGC-27 Polyclonal Cells product provides a heterogeneous pool of HGC-27 cells subjected to CRISPR/Cas9-mediated disruption of the HDAC6 gene, generating a loss-of-function model for investigating HDAC6-dependent cellular processes. This polyclonal knockout population, derived from the parental HGC-27 gastric adenocarcinoma cell line, retains the genetic background of the original tumor while abrogating HDAC6 expression, enabling studies of deacetylase activity, microtubule dynamics, and stress response pathways without clonal selection artifacts.
HGC-27 is a human undifferentiated gastric adenocarcinoma cell line originally established from a lymph node metastasis of a 75-year-old female patient. It serves as a widely used model for aggressive, invasive gastric cancer with high metastatic propensity. The metastatic origin and undifferentiated phenotype make this line particularly suitable for examining molecular mechanisms driving cancer cell dissemination, chemoresistance, and adaptation to proteotoxic stress.
HDAC6 functions as a cytoplasmic deacetylase primarily targeting acetylated ??-tubulin at Lys40, HSP90, and cortactin, with its activity regulated by upstream signals such as EGFR, Aurora A kinase, and PKC. In the knockout setting, hyperacetylation of ??-tubulin stabilizes microtubules, while impaired HSP90 deacetylation disrupts client protein maturation. These changes hinder aggresome formation by weakening interactions with p62/SQSTM1 and the dynein motor complex, and they compromise autophagy flux as indicated by altered LC3 processing. Consequently, downstream effectors including FOXP3 and peroxiredoxins are dysregulated, and pathways mediated by HDAC6??s interaction with ubiquitin, HDAC11, and SIRT2 are attenuated.
In the HGC-27 gastric cancer context, HDAC6 knockout uncovers a critical link between cytoplasmic deacetylation and metastatic fitness. Loss of HDAC6 reduces cell migration and invasion, correlating with hyperacetylated microtubules and diminished aggresome clearance. The model reveals increased susceptibility to proteotoxic and chemotherapeutic insults, offering a platform to dissect the aggresome-autophagy axis in drug resistance. Moreover, it permits evaluation of how EGFR-driven or oxidative stress-induced signaling converges on HDAC6 to modulate gastric adenocarcinoma progression.
This product enables a broad spectrum of experimental applications, including gastric cancer metastasis studies, autophagy and aggresome research, HDAC inhibitor screening, and neuroprotection models. Representative assays include Western blotting for acetylated ??-tubulin and HSP90, immunofluorescence-based aggresome detection, Transwell migration and invasion analyses, drug sensitivity assays for HDAC inhibitors, flow cytometric apoptosis quantification, and RT-qPCR profiling of autophagy markers. For further details on validation and application protocols, please contact Ascent Research.
