U-CH1

U-CH1

Cat.No.: CSC-C9258W

Species: Homo sapiens (Human)

Source: Bone

Morphology: mesenchymal like

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Cat.No.
CSC-C9258W
Description
This cell line was established from a local recurrence of a sacrococcygeal after radiotherapy 4 years after initial surgery.
Species
Homo sapiens (Human)
Source
Bone
Recommended Medium
Morphology
mesenchymal like
Disease
Sacral Chordoma
Storage and Shipping
liquid nitrogen vapor phase
Synonyms
UCH-1; UCH1
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

U-CH1 is the first validated human chordoma cell line, originally established from a recurrent sacral chordoma of a 56-year-old male patient. As the foundational model in chordoma research, U-CH1 retains classical physaliferous morphology and faithfully recapitulates the defining molecular hallmarks of chordoma. It exhibits robust nuclear expression of brachyury (TBXT)—the lineage-specific transcription factor and definitive diagnostic marker—at approximately 10-fold higher levels than U-CH2, alongside strong CD24 surface expression (13-fold higher than U-CH2). These features ensure authentic representation of chordoma biology and pathophysiology.

Genetically, U-CH1 maintains wild-type SMARCB1 status and HLA-A2 typing, with comprehensive genomic resources including publicly available whole-genome, exome, and transcriptome sequencing data. Extensively characterized and widely adopted across the research community, U-CH1 has served as the critical benchmark for establishing and authenticating subsequent chordoma cell lines.

Functionally, U-CH1 supports robust in vitro proliferation and reliably forms xenografts in immunodeficient mice, enabling integrated preclinical evaluation from mechanistic studies to in vivo drug efficacy assessment. It has been instrumental in high-throughput compound screening and in elucidating therapeutic vulnerabilities of brachyury-driven transcriptional addiction, particularly through CDK-targeted inhibition. With its authenticated origin, extensively characterized molecular profile, and proven versatility across diverse experimental platforms, U-CH1 remains the gold standard cell model for advancing chordoma biology and therapeutic development.

REGγ Promotes Proliferation and Inhibits Apoptosis of Chordoma Cells

REGγ, a proteasome activator, mediates ubiquitin-, and ATP-independent protein degradation and is overexpressed in various cancers. To determine whether REGγ regulates the occurrence and development of chordoma, Chen, Hui, et al. first established stable U-CH1 cell lines with shNC, shREGγ-1#, and shREGγ-2# (Fig. 1A, B). CCK8 assay showed that REGγ knockdown significantly inhibited U-CH1 cell proliferation (Fig. 1C). Similarly, silencing REGγ in MUG-Chor1 cells yielded the same result (Fig. 1D–F). The colony formation assay, which is commonly used to assess cell proliferation and self-renewal ability, confirmed that REGγ knockdown suppresses the proliferation of chordoma cells (Fig. 1G–J). These findings suggest that REGγ plays a key role in the occurrence and development of chordoma by modulating cell proliferation.

To investigate whether REGγ regulates chordoma by inhibiting apoptosis, they performed a cell apoptosis analysis. Using an Annexin V-APC/PI apoptosis detection kit combined with flow cytometry analysis, they observed that REGγ knockdown promoted apoptosis in U-CH1 cells (Fig. 1K, L). Western blotting revealed increased accumulation of cleaved PARP, an apoptosis marker, in REGγ-knockdown U-CH1 cells (Fig. 1O). They also observed the same phenomenon in MUG-Chor1 cells with REGγ knockdown (Fig. 1M, N). These data indicate that REGγ knockdown inhibits proliferation and promotes apoptosis in chordoma cells.

REGγ knockdown inhibits proliferation and promotes apoptosis in chordoma cells U-CH1.
Fig. 1. REGγ knockdown inhibits proliferation and promotes apoptosis in chordoma cells (Chen, Hui, et al., 2025).

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