Acriflavine inhibits the epithelial-to-mesenchymal transition in vitro in liver and pancreatic cancer cells (part of study on HepG2). Homo sapiens

Background: Epithelial-to-mesenchymal transition (EMT) is considered an important driving mechanism behind aggressive cancer phenotype. This was recently challenged by the finding that cells can metastasize without undergoing EMT. However, the same studies confirmed the important role of the EMT program in drug resistance. The EMT program is largely dependent on the cell’s microenvironment. Acriflavine (ACF) is a heteroaromatic dye with antibacterial and antiviral effects. Recently, ACF was suggested as anticancer agent for its topoisomerase inhibitor activity. ACF further blocks the hypoxia-inducible factor (HIF) pathway, an important driver of cancer aggressiveness. How ACF works in cancer is however unknown. Aim: Identification of the working mechanism, molecular pathways and signaling of ACF in EMT cancer cells. To this end, three in vitro models were developed of EMT induction (human pancreatic cancer cells stimulated with TGF-b1, human pancreatic cancer cells stimulated with CoCl2, drug resistance against sorafenib in human liver cancer cells). Only the third model - drug resistance against sorafenib in HepG2 cells - is discussed in this GEO submission. Overall design: Three conditions were investigated: (1) untreated HepG2 cells (= controls), (2) HepG2 cells treated with 2.5µM acriflavine, (3) HepG2 cells treated with 5µM acriflavine. For each condition four biological replicates were profiled.