KYSE-270

Cat.No.: CSC-C0428

Species: Homo sapiens (Human)

Source: Esophagus

Morphology: epitheloid cells growing in monolayers

Culture Properties: monolayer

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Scientific Data
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Cat.No.

CSC-C0428

Description

Derived from well differentiated invasive esophageal squamous cell carcinoma resected from middle intra-thoracic esophagus of a 79-year-old Japanese man prior to treatment (depth of invasion was not beyond the muscularis propria); described to carry p53 mutation

Species

Homo sapiens (Human)

Source

Esophagus

Recommended Medium

49%RPMI1640 + 49%Ham's F-12 + 2%h.i. FBS.

Culture Properties

monolayer

Morphology

epitheloid cells growing in monolayers

Karyotype

Human hypotriploid karyotype with 16% polyploidy - 66(64-67)<3n>XX/XXX, +1, -2, +3, -5, -6, +7, +8, -9, -10, -15, -15, -17, -18, -19, -20, -22, +5mar (1bisat), ?del(X)(q25), add(1)(p1?), add(1)(p2?), i(1p), der(1)t(1;?)(?;2)(q13;?)(?;q11), add(2)(q37), de

Disease

Esophageal Squamous Cell Carcinoma

Quality Control

Mycoplasma: contamination was eliminated with BM-Cyclin (tiamulin & minocycline), then negative in DAPI, microbiological culture, RNA hybridization assays
Immunology: cytokeratin +, cytokeratin-7 - , cytokeratin-8 +, cytokeratin-17 (+), cytokeratin-18 +,

Storage and Shipping

Frozen with 70% medium, 20% FBS, 10% DMSO at about 2 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen

Synonyms

KYSE 270; KYSE270; Kyse270; KY-270

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 KYSE-270 cell line is a well-characterized human cellular model derived from a primary esophageal squamous cell carcinoma (ESCC). ESCC is a major global health burden and the predominant histological subtype of esophageal cancer. KYSE-270, therefore, represents a highly relevant in vitro and in vivo system for studying the pathogenesis, progression, and therapeutic vulnerabilities of this aggressive malignancy. Its derivation from a primary tumor ensures it captures the genetic and phenotypic landscape of the disease at a clinically significant stage.

KYSE-270 cells exhibit typical epithelial morphology. A defining molecular feature is the presence of a nonsense mutation in the TP53 tumor suppressor gene (R213*), which is one of the most frequently mutated genes in ESCC. This loss of functional p53 contributes to genomic instability and impaired apoptosis, key hallmarks of cancer. The cell line is tumorigenic in immunocompromised mice, capable of forming solid tumors, which is essential for translational preclinical studies. It is characterized by a moderately differentiated phenotype and has been extensively profiled for its genomic, transcriptomic, and drug-response characteristics, making it a well-annotated tool in the ESCC research community.

CRISPR/Cas9 Screening Highlights PFKFB3 Gene as a Major Contributor to 5-Fluorouracil Resistance in Esophageal Cancer

Esophageal cancer (EC) is the eighth most common cancer and the sixth leading cause of death worldwide. Esophageal squamous cell carcinoma (ESCC) comprises the majority of esophageal cancers globally, and 5-Fluorouraci (5-FU) is one of the commonly used chemotherapeutics for this type of cancer. Chemoresistance is a major obstacle to the successful treatment of this malignancy.

This study used CRISPR/Cas9 screening method to determine target genes related to 5-FU drug resistance in esophageal cancer. The results showed that loss of PFKFB3 can increase 5-FU resistance in different human esophageal squamous cell carcinoma cell lines. Specifically, in KYSE-70 cells, loss of PFKFB3 induce epithelial-mesenchymal transition (EMT) and prolong the S phase of the cell cycle, enabling cancer cells to evade the effects of 5-FU and develop resistance. In KYSE-270 and KYSE-150 cell lines, loss of PFKFB3 upregulate the expression of Slug and Mcl-1, indirectly regulate Chk1 and promote its autophosphorylation, which in turn inhibits apoptosis, thus counteracting the effects of 5-FU.

Dose-response curves of esophageal cancer cell lines treated with 5-FU and their corresponding IC50 values. — Fig. 1. Knockout of PFKFB3 enhances 5-FU resistance in human esophageal cancer cell lines (Xue, Feng, *et al.*, 2025).

WT (wild-type cells), NC (transfected with non-targeting control sgRNA), sg1 (transfected with PFKFB3-sgRNA1), and sg2 (transfected with PFKFB3-sgRNA2).