CAL-85-1

Cat.No.: CSC-C0474

Species: Homo sapiens (Human)

Source: Breast

Morphology: adherent epithelial-like cells growing in monolayers

Culture Properties: monolayer

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Cat.No.

CSC-C0474

Description

Established from the relapsing invasive galactophoric breast adenocarcinoma resected from a 35-year-old woman during radiotherapy in 1990; cells were described as expressing the multidrug resistance (MDR) gene

Species

Homo sapiens (Human)

Source

Breast

Recommended Medium

90% DMEM+ 10% h.i.FBS

Culture Properties

monolayer

Morphology

adherent epithelial-like cells growing in monolayers

Karyotype

Human flat-moded hypotriploid karyotype with 8% polyploidy - 60(57-65)<3n>XX/XXX, +2, +5, -8, -10, -12, -13, -14, -15, -16, -16, -17, -18, +?20, -21, -22, +2-4mar, +fra, add(X)(q2?), del(X)(q11), add(1)(p34), del(2)(q?11q?21)x1-2, add(2)(p2?3), der(3)?inv

Disease

Breast Carcinoma

Quality Control

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

Storage and Shipping

Frozen with 70% medium, 20% FBS, 10% DMSO at about 1.5 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen

Synonyms

Cal-85-1; CAL 85-1; CAL85-1; CAL851; Centre Antoine Lacassagne-85-1

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.

CAL-85-1 was originally derived in 1990 from a 35-year-old woman who had been diagnosed with relapsing invasive ductal carcinoma of the breast. Cells display an adherent morphology that resembles epithelial-like growth. CAL-85-1 is basal-like and triple-negative (ER/PR-/HER2-) breast adenocarcinoma (TNBC) cell line with TP53 and BRCA2 mutations which are frequently altered in human breast cancer. It has been shown to have an intrinsic multidrug resistance (MDR) phenotype.

CAL-85-1 is frequently utilized in oncology high-throughput screens such as DepMap and CCLE to identify dependencies and druggable targets in TNBC. Additionally, this cell line has been used as a tool to screen novel chemotherapeutics, study DNA damage response in BRCA-deficient cells, and generate more representative 3D culture conditions/or organoids for tumor microenvironment assays.

PKM Inhibition Modulates the Radiation Response in TNBC Cells by Regulating DNA Damage Repair, Cell Cycle Progression, and DNA Replication

Metabolic reprogramming contributes to TNBC therapy resistance. Using untargeted metabolomics and a 44-gene interaction network, Matesanz-Sánchez et al. identified radiation-induced metabolic changes and nine radiosensitizing genes by RNAi screening. High PKM expression correlated with poor survival in METABRIC-TNBC; pharmacological PKM inhibition radiosensitized cells through S-phase disruption, reducing DNA synthesis while increasing replication stress and DNA damage at active forks, ultimately prolonging cell cycle arrest.

Mechanistically, combined PKMi/irradiation elevated γH2AX foci in Cal-51 and Cal-85-1 cells (Fig. 1A-B) and increased pan-nuclear γH2AX in MDA-MB-231 and Cal-85-1 cells (Fig. 1C-D), with enhanced RAD51/γH2AX colocalization (Fig. 1E). This damage was replication-dependent, shown by elevated RAD51 foci in EdU-positive MDA-MB-231 cells (Fig. 1F). Significant G2 accumulation occurred in MDA-MB-231 and Cal-85-1 cells (Fig. 1G-H), with G2 arrest correlating with pan-nuclear γH2AX and RAD51/γH2AX colocalization (Fig. 1I).

PKM inhibition modulates DNA damage repair, DNA replication, and induces cell cycle arrest in irradiated TNBC cells. — Fig. 1. PKM inhibition modulates DNA damage repair, DNA replication, and induces cell cycle arrest in irradiated TNBC cells (Matesanz-Sánchez R, Classen S, *et al.*, 2026).

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