Influenza Virus-Induced Autophagy Is Not Always Associated with MUC1 Expressions

Influenza virus-induced autophagy frequently accompanies apoptosis and results in cell death in cells infected with the virus. Autophagy has been well-known to be modulated by the mTOR/PI3K/Akt pathway, which plays an important role in response to the presence of energy sources and external stimulants. This pathway can also be modulated by MUC1, which has extracellular and intracellular components, and playing an important role in metastasis and chemotherapeutic resistance. In this study, the aim is to observe the changes in MUC1 expressions, which is known to have sialic acid residues within MUC1, therefore serving as a receptor for influenza viruses, and consequent changes in autophagy markers such as mTOR and LC3b, after inoculation of cancer cells with influenza virus. Fluorescence was detected for LC3b, mTOR and MUC1 in all influenza-positive cell lines (MCF-7, He-La, A-549) except for RD in immunofluorescence studies. In influenza-negative MCF-7, HeLa, RD and A-549 cells no fluorescence was detected. In the supernatant of all influenza-positive cells, except for RD cells, positive results were obtained for MUC1, MAP1LC3B and MTOR genes (Ct 20,01-32,04) in RT-qPCR, respectively encoding for MUC1, LC3b, and mTOR. In RT-qPCR, in cell lines without influenza inoculation, only in the A-549 cells, the gene expressions were found to be negative. In other cell lines, positive results were obtained (Ct 21,98-23,78). In RD cells, which have not been inoculated with the virus, all pathways were positive. In cells with adenocarcinoma structure, the alterations and presence of autophagy pathways and MUC1 expressions activated via influenza viruses were confirmed. However, this has not been proved using nucleic acid assays. The reason why might be the detection of only gene expressions and mRNA presence via the tests used in the study. In future studies, expressions of these genes in protein level should be detected using more advanced tests.