CAL-120

Cat.No.: CSC-C0488

Species: Homo sapiens (Human)

Source: Pleural Effusion Metastasis

Morphology: heterogenous population with epithelial-like and fibroblast-like adherent cells growing in monolayers

Culture Properties: monolayer

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Cat.No.

CSC-C0488

Description

Established from the pleural effusion of a 43-year-old woman with metastatic breast adenocarcinoma in 1991

Species

Homo sapiens (Human)

Source

Pleural Effusion Metastasis

Recommended Medium

90% DMEM+ 10% h.i.FBS

Culture Properties

monolayer

Morphology

heterogenous population with epithelial-like and fibroblast-like adherent cells growing in monolayers

Karyotype

Human hypertetraploid karyotype with 20% polyploidy 98(88-98)<4n>XXX/XXXX, -1, -2, -2, -4, +5, +5, +6, -9, -9, +10, +11, -12, -12, -13, -13, -14, -15, -16, -16, -20, -21, -22, +16-18mar, + 1-2 dmin, add(X)(p2?2), add(1)(q22), del(3)(q22), add(3)(p1?4), de

Disease

Breast Carcinoma

Quality Control

Mycoplasma: negative in microbiological culture, RNA hybridization, PCR assays
Immunology: cytokeratin +, cytokeratin-7 -, cytokeratin-8 +, cytokeratin-17 -, cytokeratin-18 +, cytokeratin-19 +, desmin -, endothel -, EpCAM +, GFAP -, neurofilament -, vimen

Storage and Shipping

Frozen with 70% medium, 20% FBS, 10% DMSO at about 1 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen

Synonyms

CAL 120; CAL120

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 CAL-120 cell line is a human breast carcinoma model isolated from a metastatic site (pleural effusion) of a primary ductal carcinoma. It holds significant niche value in oncology research as a well-characterized representative of triple-negative breast cancer (TNBC), the most aggressive and therapeutically challenging breast cancer subtype due to its lack of estrogen receptor (ER), progesterone receptor (PR), and HER2 amplification. This absence of classic hormonal and growth factor targets renders standard endocrine and HER2-targeted therapies ineffective, underscoring the critical need for models like CAL-120 to develop novel treatment strategies.

Key characteristics defining CAL-120 include its confirmed triple-negative status and basal-like phenotype, often expressing basal cytokeratins (CK5/6, CK14) and epidermal growth factor receptor (EGFR). Genomic studies indicate it carries typical genomic instability and mutational profiles associated with TNBC, making it a relevant system for studying the molecular drivers of this disease. Furthermore, it exhibits invasive and tumorigenic properties in vivo, capable of forming tumors in immunocompromised mouse models, which is essential for translational pre-clinical studies.

Fibroblast Growth Factor Receptor Signaling Modulates Cholesterol Storage in A SOAT1-Dependent Manner to Promote Mammary Tumor Cell Invasion

Signaling by fibroblast growth factor receptors (FGFRs) is active in up to 85% of breast cancers and results in enhanced proliferation, migration, and invasion of tumor cells. Here, we show that FGFR signaling regulates cholesterol metabolism in breast cancer. Specifically, we demonstrate that FGFR activation promotes cellular cholesterol storage by upregulating expression of the enzyme sterol O-acyltransferase 1 (SOAT1). Moreover, we show that inhibition of SOAT1 attenuates FGFR-mediated colony formation and invasion in tumor cells, which correlates with reduced expression of matrix metalloproteinase expression. Furthermore, we demonstrate that reducing the expression of SOAT1 in tumor cells slows the growth of mammary tumors in vivo. Taken together, the findings outline a novel metabolic function for FGFR signaling in breast cancer cells and offer additional therapeutic vulnerabilities that could be targeted in FGFR-driven cancers.

FGFR activation promotes cholesterol storage. — Fig. 1. The effects of FGFR activation on cholesterol levels in mammary tumor cells (Tuokkola, Jennifer E., *et al.*, 2025).

SOAT1 inhibition suppresses FGFR-mediated colony formation. — Fig. 2. Representative images and quantification of colony formation assays in SOAT1 inhibitor-treated HC11/R1, HC11/R1-LM1, HC11/R1-LM2 cells, 4T07 and 4T1 cells, CAL-120 cells, or Hs578T cells (Tuokkola, Jennifer E., *et al.*, 2025).

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