The HDAC6 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the HDAC6 gene in the human ovarian adenocarcinoma cell line SK-OV-3. This polyclonal format provides a heterogeneous pool of edited cells, suitable for studying the collective impact of HDAC6 loss on cancer cell biology without clonal selection artifacts. The CRISPR/Cas9-mediated gene disruption targets the HDAC6 locus, generating a loss-of-function model that abrogates HDAC6 deacetylase activity across the population.
The SK-OV-3 cell line was derived from the ascites of a patient with ovarian serous cystadenocarcinoma and serves as a well-characterized model for epithelial ovarian cancer. These cells are widely used for investigating tumorigenesis, drug resistance, and metastatic progression, making them an ideal host for evaluating the functional roles of genes like HDAC6 in ovarian cancer biology.
HDAC6 is a cytoplasmic deacetylase that removes acetyl groups from lysine residues on substrates such as ??-tubulin, Hsp90, and cortactin. This modulates microtubule stability and dynamics, Hsp90 chaperone activity, and actin polymerization, thereby regulating cell motility and protein quality control. HDAC6 functions in the aggresome-autophagy pathway by linking ubiquitinated misfolded proteins to dynein motors via p97/VCP and ubiquitin, facilitating their retrograde transport and degradation. Upstream regulators including STAT3, NF-??B, HIF-1??, and EGFR signaling modulate HDAC6 expression, while its activity directly impacts downstream effectors such as acetylated ??-tubulin, Hsp90, and cortactin, intersecting with microtubule dynamics, cell migration signaling, and protein degradation pathways.
In SK-OV-3 ovarian cancer cells, HDAC6 knockout leads to hyperacetylation of ??-tubulin, resulting in stabilized but less dynamic microtubules, impaired cell motility, and altered EGFR trafficking. Disruption of Hsp90 deacetylation compromises chaperone function, potentially sensitizing cells to proteasome inhibition and affecting oncogenic client proteins. HDAC6 is implicated in epithelial-mesenchymal transition and platinum resistance, and its interaction with TGF-?? signaling further promotes cancer progression and metastasis. This polyclonal knockout model thus provides a valuable tool to dissect HDAC6-dependent oncogenic mechanisms in ovarian cancer.
This knockout cell population is suitable for a range of assays including western blotting for acetylated ??-tubulin, Transwell migration/invasion assays, and immunofluorescence for microtubule organization. Additional applications encompass immunoprecipitation of HDAC6 interactors, flow cytometric cell cycle analysis, MTT viability assays, RT-qPCR profiling of target genes, and HDAC activity measurements. Researchers can utilize these cells to explore ovarian cancer progression, cytoskeletal dynamics, protein degradation mechanisms, and chemoresistance. For further technical details, please contact Ascent Research.
