Ca9-22

Cat.No.: CSC-C6348J

Species: Homo sapiens (Human)

Source: Oral Cavity; Gingiva

Morphology: epithelial-like

Culture Properties: Adherent cells

  • Specification
  • Background
  • Scientific Data
  • Q & A
  • Customer Review
Cat.No.
CSC-C6348J
Description
Human gingival carcinoma cell line. Expressing remarkable EGF receptor. HLA-A 2/24.
Species
Homo sapiens (Human)
Source
Oral Cavity; Gingiva
Recommended Medium
Culture Properties
Adherent cells
Morphology
epithelial-like
Disease
Gingival Squamous Cell Carcinoma
Storage and Shipping
Ship in dry ice.
Store in liquid nitrogen.
Synonyms
CA9-22; Ca 9-22; CA922; Ca922
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.

The Ca9-22 cell line is a human-derived epithelial model established from a gingival squamous cell carcinoma (OSCC) of the lower jaw. It serves as a specific and valuable tool for studying malignancies originating from the oral cavity, particularly those arising from the gingiva. Genomically, it carries mutations typical of OSCC, most notably a frequently cited TP53 mutation (R248L), which contributes to loss of tumor suppressor function and genomic instability. Phenotypically, it exhibits adherent, epithelial-like growth and forms moderately differentiated tumors in immunocompromised mice.

Current studies leveraging the Ca9-22 cell line focus on several key areas of oral oncology:

Molecular Pathogenesis of OSCC: Investigating the functional consequences of specific genetic alterations (e.g., mutant TP53 signaling) on cell cycle control, apoptosis, and the crosstalk with oncogenic pathways like PI3K/AKT.

Drug Repurposing and Novel Compound Screening: Serving as one of several OSCC cell lines in panels to screen for the efficacy of novel small molecules, natural compounds, or repurposed drugs targeting proliferation, survival, or sensitization to radiotherapy.

Angiogenesis and Tumor Microenvironment: Studying the expression and regulation of pro-angiogenic factors (e.g., VEGF) by OSCC cells and their paracrine effects on endothelial cells.

Biomarker Discovery and Validation: Used as a model system to validate the functional role of candidate genes or non-coding RNAs (e.g., miRNAs, lncRNAs) identified from clinical OSCC samples as promoters or suppressors of malignant phenotypes.

Selective Efficacy of Hydroxychloroquine on Gingival Squamous Cell Carcinoma

Oral cancer, the most common head and neck malignancy, has a high recurrence rate and poor prognosis largely owing to chemotherapy resistance. The adverse effects of conventional therapies have prompted investigations into safer and more effective alternative therapies. Chloroquine (CQ) and hydroxychloroquine (HCQ) have shown potential owing to their roles in autophagy modulation and immune regulation. This study clarifies the selective efficacy of CQ and HCQ in oral squamous cell carcinoma models, emphasizing distinct responses in gingival (Ca9-22) and tongue (SCC-9) carcinoma cells.

HCQ significantly reduced viability and colony formation in Ca9-22 cells while moderately affecting SCC-9 cells. Autophagy inhibition was accompanied by compensatory up-regulation of autophagy-related genes, consistent with feedback activation of TFEB and FOXO3a pathways. Gene expression profiling and flow-cytometry analyses revealed cell-type-specific differences in apoptosis, mitochondrial potential, and DNA damage, suggesting HCQ's selective anti-tumor potential in gingival carcinoma. These findings highlight HCQ as a repurposed adjuvant therapy that modulates autophagy and apoptosis to enhance chemosensitivity in oral cancer.

Apoptosis in Ca9-22 and SCC-9 after treated with CQ and HCQ for 24 h.

Fig. 1. Effect of CQ and HCQ on apoptosis induction (Baroudi, Sana, et al., 2025).

Ask a Question

Write your own review

  • You May Also Need

For research use only. Not for any other purpose.

Hot Products