BETA-TC-3

Cat.No.: CSC-C1092

Species: Mus musculus (Mouse)

Source: Pancreas

Morphology: adherent cells growing as multilayers

Culture Properties: multilayer

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Cat.No.
CSC-C1092
Description
Established from pancreatic insulinoma excised from a transgenic mouse carrying hybrid insulin-SV40 large T genes in 1988; described as producing pro-insulin I and II processed into mature insulin (inducible 30-fold by glucose); however, the Creative Bioarray did not verify the production of insulin
Species
Mus musculus (Mouse)
Source
Pancreas
Recommended Medium
82.5% DMEM + 15% horse serum. + 2.5% h.i.FBS
Culture Properties
multilayer
Morphology
adherent cells growing as multilayers
Karyotype
Murine hypotetraploid karyotype - 74(70-78)<4n> - 2-4 centric fusion markers and 1-3 dmin present
Disease
Mouse Insulinoma
Quality Control
Mycoplasma: negative in DAPI, microbiological culture, RNA hybridization assays
Viruses: ELISA: reverse transcriptase positive; PCR: SMRV -
Storage and Shipping
Frozen with 70% medium, 20% FBS, 10% DMSO at about 2.5 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen
Synonyms
Beta-TC-3; beta-TC-3; beta-TC3; beta TC3; BETATC3; BetaTC3; betaTC3; bTC3
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.

Beta-TC-3 is a pancreatic β-cell line from mice, originally isolated from insulinomas that spontaneously developed in transgenic mice carrying a chimeric insulin-promoter-driven SV40 large T antigen. Beta-TC-3 retains important characteristics of the differentiated β-cell. Beta-TC-3 can be grown as an adherent, transformed, yet genetically stable cell line in culture, and has a doubling time of approximately 34 hours.

Beta-TC-3 has been shown to express and process proinsulin I and II to the same degree as mature insulin as is observed in normal islet β-cells, and secretion of insulin from Beta-TC-3 can be stimulated several fold (up to ~30-fold) by glucose, although the threshold to achieve maximum release is lower than that of primary β-cells. In addition to insulin, Beta-TC-3 also shows high expression of other pre-prohormone mRNAs, including pro-Dynorphin. Stimulation (e.g. cAMP analogues) can also induce production and secretion of opioid peptides derived from pro-Dynorphin. This feature has made Beta-TC-3 a unique cell line to study not only insulin biosynthesis and glucose-stimulated secretion, but also prohormone processing and alternative peptide production in β-cells.

Beta-TC-3 is widely used today as an in vitro system to study β-cell biology, regulation of insulin gene expression and secretory dynamics, prohormone processing, and for screening of pharmacological agents affecting β-cell function, due to its stability in growth and replicability as well as maintained β-cell functions.

FAKi Induce Dephosphorylation at Tyr-397 of FAK in Pancreatic Tumor Cells

Pancreatic ductal adenocarcinoma (PDAC) is highly aggressive with a dense stroma and immunosuppressive tumor microenvironment. FAK inhibitors (FAKi) show promise in cancer treatment but have modest effects as monotherapy. Geisler et al. investigated the cytotoxicity of six FAKi on pancreatic tumor cell lines and explores their combination with the oncolytic virus CVB3 strain PD-H to enhance anti-tumor activity. To verify their functionality in pancreatic cancer cells, the Beta-TC-3 cell line was treated with 10 µM or 30 µM of different FAKi. After 24 hours, proteins were isolated and analyzed by Western blotting for levels of Tyr-397 phosphorylated FAK, total FAK, and β-actin (loading control). Results showed dephosphorylation of Tyr-397 when cells were treated with 10 µM FAKi, and more so with 30 µM. VS-4718, Ifebemtinib, and CEP-37440 were the most potent, while VS-6062 and Defactinib had moderate effects and GSK2256098 had minimal activity. Total FAK protein levels also decreased (Fig. 1). These findings confirm that all tested FAKi inhibit Tyr-397 phosphorylation in pancreatic tumor cells, with varying degrees of effectiveness.

Detection of Tyr-397 phosphorylated FAK and total FAK levels in Beta-TC-3 cells following treatment with FAKi.

Fig. 1. Detection of Tyr-397 phosphorylated FAK and total FAK levels in Beta-TC-3 cells following treatment with FAKi (Geisler A, Dieringer B, et al., 2025).

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