CAL-62

Cat.No.: CSC-C0480

Species: Homo sapiens (Human)

Source: Thyroid Gland

Morphology: epithelial-like cells growing in monolayers

Culture Properties: monolayer

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Cat.No.

CSC-C0480

Description

Established from the thyroid gland (right lobe) of a 70-year-old woman with thyroid anaplastic carcinoma in 1988; described as being tumorigenic in heterotransplanted nude mice

Species

Homo sapiens (Human)

Source

Thyroid Gland

Recommended Medium

90-95%DMEM + 5-10% h.i.FBS

Culture Properties

monolayer

Morphology

epithelial-like cells growing in monolayers

Karyotype

Human, flat-moded hypertriploid karyotype with 8% polyploidy - 60-76<3n>XX, -X, +3, +3, -4, +6, +7, +9, -11, -14, -18, +19, +20, +20, +2-6mar - del(1)(p34), der(1)t(1;17)(p34;q21), der(3)add(3)(p11)?dup(3)(q21q22)x2-4, del(6)(q15)x2, i(8q), der(?12)t(1;12

Disease

Thyroid Gland Anaplastic 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 5 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen

Synonyms

Cal-62; CAL 62; Cal 62; CAL62; Centre Antoine Lacassagne-62

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-62 is a human ATC cell line originally derived from the right lobe tumor of a 70-year-old female patient. These cells exhibit epithelial-like, adherent morphology in vitro and forms aggressive, tumorigenic xenografts in immunodeficient mice, and has become a widely used experimental model for the biology of aggressive thyroid cancer. The line has a relatively short population doubling time and exhibits cytogenetic complexity as expected for a high-grade tumor. Key oncogenic alterations were identified in this line during genomic profiling, most notably a KRAS p.G12R mutation, as well as additional alterations in genes such as EP300 and CREBBP.

Phenotypically, CAL-62 has been shown to often lack classical markers of thyroid differentiation (e.g. thyroglobulin) and exhibit mesenchymal-like, migratory features typical of dedifferentiated ATC cells. Functionally, it has been used to study pathways involved in proliferation, invasion, metabolic reprogramming, and resistance to therapy, including radioresistance (reported in one of the earliest characterization studies of this line). Because this cell line is extensively profiled in genomic, transcriptomic, proteomic, and pharmacologic public datasets, it is an ideal model for mechanistic studies and preclinical testing of candidate therapeutics.

LARS1 Knockdown Decreases the Proliferation and Increases the Apoptosis of TC Cells

Given the elevated prevalence of thyroid cancer in China and its status as the leading malignant endocrine tumor, identifying molecular targets for intervention is critical. Jin's team sought to define the functional significance of LARS1 in thyroid cancer pathogenesis and delineate the mechanistic pathways involved.

Immunohistochemical analysis showed that LARS1 protein levels were much higher in thyroid carcinoma (TC) tissues than in adjacent non-cancerous tissues. This suggests that elevated LARS1 expression may contribute to TC development and progression. CCK-8 analysis revealed significantly reduced growth in LARS1-silenced CAL-62 and 8305C cells compared to controls (Fig. 1A). EdU incorporation analysis also showed a significant decrease in replicating cells after LARS1 knockdown (Fig. 1B). Flow cytometry showed a significant increase in apoptotic cells in LARS1-silenced CAL-62 and 8305C lines compared to controls (Fig. 2A). TUNEL assays confirmed this, with a significant rise in DNA fragmentation-positive cells in the si-LARS1 group compared to controls (Fig. 2B).

Cell proliferation in difference groups, NC: The cells were treated with normal; si-NC: The cells were transfected with si-NC (negative control); si-LARS1: The cells were transfected with si-LARS1 which inhibitor LARS1 ACell proliferation rate by CCK-8 assay BEdU-positive cell number by EdU staining. — Fig. 1. Cell proliferation in difference groups, NC: The cells were treated with normal; si-NC: The cells were transfected with si-NC (negative control); si-LARS1: The cells were transfected with si-LARS1 which inhibitor LARS1 ACell proliferation rate by CCK-8 assay BEdU-positive cell number by EdU staining (Jin C W, Li C H, *et al.*, 2025)

Cell apoptosis in difference groups, NC: The cells were treated with normal; si-NC: The cells were transfected with si-NC (negative control); si-LARS1: The cells were transfected with si-LARS1 which inhibitor LARS1 ACell apoptosis rates in difference groups by flow cytometry BTUNEL positive cell number by TUNEL staining. — Fig. 2. Cell apoptosis in difference groups, NC: The cells were treated with normal; si-NC: The cells were transfected with si-NC (negative control); si-LARS1: The cells were transfected with si-LARS1 which inhibitor LARS1 ACell apoptosis rates in difference groups by flow cytometry BTUNEL positive cell number by TUNEL staining (Jin C W, Li C H, *et al.*, 2025)

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For research use only. Not for any other purpose.