BioProject

Microarray analysis was carried out on human SUIT2 cells exposed to P-bi-TAT (10-6 M tetrac equivalent) for 24 h. More...

Microarray analysis was carried out on human SUIT2 cells exposed to P-bi-TAT (10-6 M tetrac equivalent) for 24 h. P-bi-TAT significantly downregulated electron transport chain genes ATP5A1 (ATP synthase A1), ATP51, ATP5G2, COX6B1 (cytochrome c oxidase subunit 6B1), NDUFA8 (NADH dehydrogenase [ubiquinone] FA8), NDUFV2 and other NDUF genes, SLC25A6 (solute carrier group 2), UCP2 ([mitochondrial] uncoupling protein 2) and COX5A. The NDUF and ATP genes are also relevant to control of oxidative phosphorylation and transcription. Six additional NDUF genes linked to oxidative phosphorylation were affected. Conclusions. P-bi-TAT caused downregulation of expression of a panel of genes involved in electron transport, oxidative phosphorylation, and cytoplasmic ribosomal protein generation in GBM cells. A key component of the anticancer activity of P-bi-TAT relates to disordering of ATP generation mechanisms in tumor cells. Overall design: Studied the anticancer functions of P-bi-TAT in SUIT cells in terms of modulation of transcription by the drug of genes essential to cancer cell mitochondrial function. Compared with triplicate SUT2 cells with SUIT2 cells treated with P-bi-TAT (30 µM) for 24 h. Less...