GSU

Cat.No.: CSC-C6317J

Species: Homo sapiens (Human)

Source: Ascites Metastasis

Morphology: other

Culture Properties: Adherent cells

Inquire for Price

Specification
Background
Scientific Data
Q & A
Customer Review

Cat.No.

CSC-C6317J

Description

Human cell line derived from gastric cancer. Established from the cells in ascites.

Species

Homo sapiens (Human)

Source

Ascites Metastasis

Recommended Medium

RPMI-1640 + 10% h.i. FBS

Culture Properties

Adherent cells

Morphology

other

Disease

Gastric Carcinoma

Storage and Shipping

Ship in dry ice.
Store in liquid nitrogen.

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 GSU cell line is a human cell line derived from gastric cancer, specifically established from the cells present in the ascitic fluid of a patient with this malignancy. Ascites can contain cancer cells that have detached from the primary tumor, providing a rich source of malignant cells for cell line development. The GSU cell line has been characterized by its growth properties, genetic profile, and phenotypic traits, making it a valuable tool for cancer research.

The GSU cell line was created to provide a reliable and reproducible model system for studying the biology of gastric cancer. In the laboratory, GSU cells exhibit characteristics typical of gastric cancer cells, such as rapid proliferation, the ability to form colonies in soft agar, and the expression of specific biomarkers associated with gastric cancer. These cells can be cultured in vitro, allowing researchers to perform a variety of experiments to investigate the effects of genetic mutations, drug treatments, and other interventions on gastric cancer cell behavior.

Trastuzumab and Cetuximab Sensitivity of Gastric Cancer Cell Lines

A panel of 11 gastric cancer cell lines was used. Following treatment with 10 µg/ml cetuximab, GSU cells displayed a decrease in cell proliferation to 68.10% in comparison with the untreated control (p = 0.04). H111TC cells were less sensitive with growth rates of 82.30% after treatment with 10 µg/ml cetuximab (p = 0.002) and a maximum inhibition of 80.16% after application of 200 µg/ml (p < 0.001). MKN7 cells showed only a minor sensitivity with a maximum decrease of cell proliferation to 83.63% following treatment with 100 µg/ml cetuximab (p = 0.001). HGC-27 cells were completely resistant to cetuximab.

Additionally, the trastuzumab sensitivity of the cell lines was investigated via cell proliferation assay (Fig. 1). Two cell lines were identified as trastuzumab sensitive: GSU and H111TC. Both displayed a significant decrease in cell proliferation after the application of the therapeutic. For GSU, 0.1 µg/ml was already sufficient to inhibit the proliferation rate to 80.10% (p = 0.009), while 40 µg/ml caused an inhibition of 72.98% (p = 0.002). H111TC displayed a less sensitive phenotype with a maximum inhibition of 80.03 and 80.31% after application of 20 µg/ml and 40 µg/ml trastuzumab (p = 0.024; p = 0.02), respectively. For the other cell lines, no significant inhibition of cell proliferation was observed.

Table 1. Effect of cetuximab treatment on the gastric cancer cell lines. (Kneissl J, et al., 2017)