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Transfection Reagent for Calu-6 Cells (Lung Carcinoma Cell, HTB-56)

The Calu-6 (ATCC number HTB-56) epithelial cell line was derived from the tissue of a 61-year-old Caucasian female suffering from anaplastic carcinoma (lung cancer). The Calu-6 transfection cells are used for research models to further study human lung cancer and its leading pathways. Additionally, research on the relationship between animycin A (AMA) and lung cancer cells have also been conducted. Calu-6 transfection reagents enhance the intracellular delivery of oligonucleotides when the Calu-6 cell line is used as a transfection host. 

Transfection Reagent for Calu-6 Cells (Lung Carcinoma Cell, HTB-56)

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Calu-6 Cell Line

The Calu-6 cell line was established from the lung tissue of a 61-year-old Caucasian female who had been suffering from anaplastic carcinoma. Calu-6 cells are tumorigenic and have a modal chromosome number of 59. They also exhibit adherent cultural properties and display an epithelial morphology. The Calu-6 cell line is a suitable transfection host for in vivo and in vitro  methods to study lung cancer, and a Calu-6 Transfection Reagent  can be purchased through Altogen Biosystems  to transfect Calu-6 cells. A Calu-6 xenograft model can be found here . 

The Role of Vandetanib in Calu-6 Cells

Vandetanib is a multikinase inhibitor that is a target of drug treatments for non-small cell lung cancer. In this study, researchers determine the cellular and biological effects of vandetanib on Calu-6 cells. Results showed that vandetanib inhibits Calu-6 cell migration and invasiveness. Vandetanib also induces autophagy in Calu-6 cells by increasing the level of reactive oxygen species (ROS). These findings show that vandetanib produces a double effect in some NSCLC cells, which presents vandetanib as a potential agent for treatment of Calu-6 cells. [ LINK ]

Effects of Cediranib Treatment on Calu-6 and Calu-3 Cells

Tumors are characterized by either tumor vessel or stromal vessel phenotypes, which reportedly define how tumors responds to VEGFR2 antibody treatment. In this study, researchers seek to understand whether the tumor phenotypes associate with vascular response to VEGFR tyrosine kinase inhibitors (TKI) or if changes in vascular function are associated with changes in tumor size. Stromal vessel phenotype Calu-3 and tumor vessel phenotype Calu-6 cells were treated with cediranib for 5 days. Following treatment, cediranib decreased Calu-3 tumor perfusion and hypoxia significantly increased; however, neither of these factors were affected in Calu-6 tumors. These findings suggest that tumor stromal phenotypes associate more with acute tumor vascular response to VEGFR TKI. [ LINK ]