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There is accumulating evidence indicating that microRNA (miR)-9-3p expression is abnormal in patients with glioma; however, the role of miR-9-3p in glioma remains unclear. In the present study, reverse transcription-quantitative PCR and immunohistochemical assays were conducted to assess miR-9-3p and forkhead box G1 (FOXG1) expression, respectively. A luciferase reporter assay was performed to confirm the target of miR-9-3p. Moreover, cell counting kit-8 and flow cytometry assays were used to assess proliferation and apoptosis, respectively. The present study demonstrated that miR-9-3p is significantly downregulated, and FOXG1 is significantly upregulated, in patients with glioma. miR-9-3p overexpression inhibited proliferation and increased the apoptosis of both U87MG and TG-905 cells. In addition, FOXG1 was identified as a direct target of miR-9-3p, and FOXG1 silencing enhanced the inhibitory effect of miR-9-3p on proliferation and apoptosis in U87 MG and TG-905 cells. In conclusion, the present results suggest that miR-9-3p may suppress malignant biological properties by targeting FOXG1. Thus, miR-9-3p may serve as a diagnostic target and novel prognostic marker in patients with glioma.

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The synthesis of phospholipids relies on a sort of genes, whose promoter regions contain inositol-sensitive upstream activation sequence (UAS INO) and are regulated by the basic helix-loop-helix (bHLH)-type ino2/ino4 transcription factor (TF) pair. Ten putative bHLH TFs have been found through whole genome sequencing of Aspergillus niger, but none of these TFs have been characterized. In this study, we identified and characterized the bHLH-type TF ino2(An02g04350) in A. niger. Electrophoretic mobility shift assay (EMSA) and yeast two-hybrid assay demonstrated that ino2 functions as a homodimer in UAS INO genes (e.g., ino1 and cho1) and binds to opi1(An1g02370) in vitro. Real-time quantitative PCR of ino1 and quantification of total phospholipid indicated that the ino2 disruptant downregulated the transcription of ino1 and the amount of total cellular phosphatidylinositol. In addition, phenotype analyses showed that a loss of ino2 led to resistance to cell wall interference and DNA damage. Comparative transcriptome analyses showed that more than 1000 genes and GO terms associated with UAS INO , endoplasmic reticulum-associated protein degradation, phosphatidylinositol synthesis, chitin synthesis, and fatty acid synthesis were differentially expressed in ino2 compared to the wild type (WT). Taken together, these observations indicate that the bHLH TF ino2 functions as a homodimer that regulates the synthesis of phosphatidylinositol, fatty acid, and chitin and influences the homeostasis of the endoplasmic reticulum membrane.