In Stock Cell Lines
The PSME3 Knockout HCS?2/8 Cell Line is a CRISPR/Cas9?edited human chondrosarcoma knockout cell line lacking the proteasome activator PA28??. PSME3 facilitates ubiquitin?independent degradation of p53, p21, and SRC?3 downstream of p53 and NF???B, and its disruption stabilizes these tumor suppressors, enabling detailed study of proteasome?regulated cell cycle control and apoptosis in a cartilage?producing chondrosarcoma model. This model is widely applicable in cancer biology, drug resistance screening, and proteostasis research, and is compatible with assays such as western blotting, RT?qPCR, proteasome activity assays, cell cycle analysis by flow cytometry, and colony formation assays to evaluate PSME3?dependent phenotypes.
CLIC1 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG17421
NSUN6 Knockout HT29 Polyclonal Cells
Cat. No. ARG13850
MACF1 Knockout A549 Polyclonal Cells
Cat. No. ARG10666
C1orf159 Knockout HEK293T Polyclonal Cells
Cat. No. ARG37723
CSNK1G3 Knockout HCT116 Polyclonal Cells
Cat. No. ARG7055
Mouse Gallbladder Epithelial Cells
Cat. No. ARP0473
The PSME3 Knockout HCS?2/8 Cell Line is a CRISPR/Cas9?edited human knockout cell line with disrupted PSME3 expression. Derived from the HCS?2/8 chondrosarcoma line, it provides a stable loss?of?function model for investigating proteasome activator subunit PA28??. Supplied as an edited cell line, it enables reproducible studies of PSME3-dependent ubiquitin?independent proteolysis without transient silencing.
The parental HCS?2/8 cell line is a widely used human chondrosarcoma model that retains cartilage extracellular matrix production, closely mimicking the tumor microenvironment. Chondrosarcomas are malignant cartilage tumors with limited therapies, and this line is essential for studying tumor biology, matrix homeostasis, and drug sensitivity. The knockout line extends its utility by allowing dissection of PSME3??s role in chondrosarcoma pathophysiology.
PSME3 (PA28??) forms the 11S activator complex that binds the 20S proteasome to stimulate ubiquitin?independent degradation of key cell cycle and survival regulators. It acts downstream of p53 and NF???B and is activated by oncogenic stress; it targets p53, p21, SRC?3, cyclin D1, and c?Myc for degradation. PSME3 interacts with MDM2 to facilitate p53 turnover, linking proteasomal activity to tumor suppression. Loss of PSME3 thus stabilizes these substrates, inducing cell cycle arrest and apoptosis. This knockout cell line offers a clean genetic system to map PSME3?dependent signaling through the p53/MDM2 and MAPK/ERK pathways.
In chondrosarcoma, PSME3 overexpression drives proliferation and chemoresistance via constitutive p53 degradation. By deleting PSME3 in HCS?2/8 cells, this model restores p53 function, enabling studies of p53?dependent apoptosis, p21?mediated growth arrest, and altered drug responses. The cartilage matrix?producing capability of HCS?2/8 cells allows investigation of proteasome?matrix crosstalk, shedding light on how proteolytic regulation influences cartilage tumor progression and matrix integrity.
Typical applications include western blotting and RT?qPCR to validate knockout and assess downstream targets; proteasome activity assays to measure 20S function; proliferation (MTT/BrdU) and colony formation assays for growth phenotypes; flow cytometry for cell cycle and apoptosis (Annexin V) analyses; and co?immunoprecipitation to examine interactions with MDM2 and 20S complex. This line also supports drug resistance profiling and mechanistic studies of p53 re?expression. For further information, contact Ascent Research.
