KYSE-410

Name: KYSE-410
Brand: Creative Bioarray

Cat.No.: CSC-C0429

Species: Homo sapiens (Human)

Source: Esophagus

Morphology: epitheloid adherent cells growing in monolayers

Culture Properties: monolayer

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Cat.No.

CSC-C0429

Description

Established from the poorly differentiated invasive esophageal squamous cell carcinoma resected from the cervical esophagus of a 51-year-old Japanese man prior to treatment (tumor invasion into the adventitia was obvious); described to overexpress hst-1 (= heparin-binding growth factor) and cyclin D1

Species

Homo sapiens (Human)

Source

Esophagus

Recommended Medium

90-95% RPMI-1640 + 5-10% h.i. FBS

Culture Properties

monolayer

Morphology

epitheloid adherent cells growing in monolayers

Karyotype

Human flat-moded hypotetraploid karyotype with 4% polyploidy - 79-91<4n>Xder(X), -10, -18, -19, -21, -22, -22, +6mar, add(X)(qter), add(1)(p11)/del(1)(p13), add(3)(q21)x1-2, add(5)(p13), der(6)t(4;6)(q12;q14)x1-2, dup(7)(p12p14), der(7)del(7)(p12p21)t(7;9

Disease

Esophageal Squamous Cell Carcinoma

Quality Control

Mycoplasma: contamination was eliminated with Ciprobay (ciprofloxacin), then negative in DAPI, microbiological culture, RNA hybridization assays
Immunology: cytokeratin +, cytokeratin-7 +, cytokeratin-8 +, cytokeratin-17 +, cytokeratin-18 +, cytokeratin-

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

KYSE 410; KYSE410; Kyse410; KYSE0410

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.

KYSE-410 is a rigorously authenticated human esophageal squamous cell carcinoma (ESCC) cell line established from a poorly differentiated invasive primary tumor resected from the cervical esophagus of a 51-year-old patient prior to treatment. As a founding member of the extensively characterized KYSE series, it offers exceptional model fidelity for ESCC research.

Molecularly, KYSE-410 is distinguished by epigenetic silencing of the p16 (INK4a) tumor suppressor via 5' CpG island hypermethylation while retaining wild-type p15 (INK4b)—a selective inactivation pattern representative of specific ESCC subtypes. The line further harbors pathogenic TP53 and KRAS mutations, MYC amplification, and robust overexpression of hst-1 (heparin-binding growth factor) and cyclin D1, faithfully recapitulating key oncogenic drivers and proliferative signaling circuits.

Cytogenetically, KYSE-410 exhibits a hypotetraploid karyotype with authenticated STR profiling. It demonstrates confirmed tumorigenicity in athymic nude mice, with resultant tumors displaying classical ESCC histology. With comprehensive molecular annotation, standardized culture protocols, and proven utility across in vitro and in vivo platforms, KYSE-410 remains a cornerstone model for investigating ESCC biology, epigenetic therapeutics, and drug development.

The Mechanism of HMGB1 in the Proliferation and Macrophage Polarization in Esophageal Squamous Cell Carcinoma Cells

Previous studies showed that high mobility group box-1 (HMGB1) facilitates the initiation and progression of esophageal squamous cell carcinoma (ESCC), and the current research investigated the detailed mechanisms implicated.

Quantitative real-time PCR (qRT-PCR) was performed to detect the expressions of HMGB1 in both human esophageal epithelial cells (HEEC) and ESCC cells. After cell transfection, the proliferation of ESCC cells was measured, and the cell metastasis was determined based on the levels of cadherins (CDHs) and Vimentin (VIM). Macrophage polarization was determined by calculating the mean fluorescence intensity (MFI) of CD206 and CD86.

HMGB1 showed a higher expression in ESCC cells, while knockdown of HMGB1 inhibited ESCC cell proliferation, downregulated the levels of CDH2 and VIM and upregulated the level of CDH1. In contrast, overexpressed HMGB1 showed the opposite effects, suggesting the role of HMGB1 in the epithelial–mesenchymal transition (EMT) of ESCC. After the knockout of HMGB1, the MFI of CD86 was increased but that of CD206 was reduced, indicating the polarization towards M1 macrophages. However, the results were reversed when HMGB1 was overexpressed.