ral and cellular origins were shown to affect cellular GSK-126 site responses to viruses such as apoptosis, therefore, it is possible that autophagy-regulating miRNAs play a role in the battle between viruses and the host. In line with a possible role of MIR376 family in virus-host interactions, a miRNA profiling MIR376A Regulation of Starvation-Induced Autophagy revealed differential expression of MIR376A and MIR376B in control versus HIV-1 positive peripheral blood mononuclear cells. In another study, an interesting interplay between viral miRNAs and MIR376A was reported. MREs for MIR376A in the 39 UTR of the MICB mRNA overlapped with the MRE of Kaposi’s sarcoma-associated herpesvirus miRNA, miR-K12-7. The MIR376A MRE was also in the vicinity of that of miR-UL112 of human cytomegalo virus. Surprisingly, when MIR376A was used in combination with KSHV or HCMV miRNA, no antagonism but an increase in target MICB downregulation was observed. In the light of our data, here contribution of MIR376A 
to viral infection might not be limited to the attenuation of immune responses through MICB downregulation, but it might also involve blockage of antiviral autophagic degradation, autophagy-related antigen 20354118 presentation on MHC molecules and perhaps autophagic cell death. Indeed, KSHV was previously shown to downregulate autophagy, apoptosis and cell death using its viral FLIP and BCL-2 proteins that target autophagy-related proteins ATG3 and BECN1, respectively. MIR376A and possibly other autophagy-regulating miRNAs might be usurped by viruses to overcome the antiviral effects of autophagy. Altogether, our results underline the importance of MIR376A and MIR376B, and miRNAs in general, in the control of autophagic responses of cells and tissues. miRNA-mediated regulation provides a flexible and dynamic mechanism for the regulation of autophagy under various stress conditions, and adds another layer of regulation for critical cell death and survival decisions in 20573509 health and disease. Quantitative GFP-LC3 analyses 48h post-transfection, GFP-LC3 dot positivity was quantified following 2 hours or 4 hours starvation in the EBSS medium. 10 or 15 GFP-LC3 dots per cell were considered as a threshold for the basal autophagic activity in MCF-7 and Huh7 cells, respectively. Minimum 150 GFP positive cells were counted under each condition, and percentage of GFPLC3 positivity was expressed as a percentage of GFP-LC3 dot positive cells within the total transfected cell population. miRNA target prediction Bioinformatics tools, Microcosm Targets, and MiRanda were utilized to determine miRNA potential target mRNAs. Immunoblotting and antibodies Protein extracts from cells were prepared and immunoblotted as previously described using antibodies specific to BECN1, LC3B, ATG4C, SQSTM1 and ACTB. ImageJ software was used to quantify protein band intensities. RNA isolation, RT-PCR analysis and Real-time RT-PCR Total RNA was extracted using TRIzol reagent according to the manufacturer’s instructions. SYBRH Green Quantitative RT-PCR kit was utilized for single step qRT-PCR reactions. The 22nnCT method was applied for the quantification of mRNA changes, and GAPDH mRNA was used as control. Reactions were performed in duplicates and independent experiment repeat numbers were marked. Materials and Methods Plasmid constructs The pMSCV-blast-miR plasmids, containing either hsa-miR376a1 human miRNA or control miRNA, were constructed as described previously. For luciferase tests, miRNA response el