Glioma is one of the most treatment‐refractory intracranial tumors, and the aberrant expressed Wnt/β‐catenin pathway is closely associated with glioma malignancy. In this regard, Wnt/β‐catenin signaling has been reported to play an essential role in cellular proliferation, migration, invasion, and angiogenesis, therefore contributing to glioma progression. However, the underlying mechanisms of Wnt/β‐catenin signaling involvement in gliomagenesis remain unknown. Here, we present an overview of the Wnt components and then go on to summarize the current knowledge describing the multitude of roles of Wnt/β‐catenin in glioma, which are mediated by transcription factors, microRNAs, long noncoding RNAs, and so on. In the latter portion of the review, we elaborate the increasing apparent crosstalk of Wnt/β‐catenin pathway with PI3K/AKT signaling involved in these processes. Ultimately, compounds targeting the Wnt/β‐catenin are described in glioma. As better understanding of the regulatory mechanisms to glioma malignancies increases, Wnt/β‐catenin cascade may represent an area of developmental glioma therapeutics focus.

Cholesterol accumulation is a critical step during the development and progression of atherosclerosis. Recently, Wnt5a expression has been found to be markedly upregulated in both murine and human atherosclerotic lesions. However, the effect and mechanism of Wnt5a in atherosclerosis is poorly understood. In the present study, we investigated the effects and potential mechanisms of Wnt5a on cholesterol accumulation during atherosclerosis. We used RAW264.7 and vascular smooth muscle cells (VSMC) treated with oxidized low-density lipoprotein (oxLDL) as lipid-loaded cell models. We found that expression of Wnt5a protein was increased in a concentration (25, 50, 75 and 100 μg/mL)- and time (24, 48 and 72 h)-dependent manner by oxLDL treatment. To explore the underlying mechanism, we used Wnt5a short interference (si) RNA to knockdown Wnt5a expression in both RAW264.7 cells and VSMC, or applied recombinant Wnt5a (rWnt5a) to stimulate Wnt5a signalling. After Wnt5a knockdown, total cholesterol (TC) and free cholesterol (FC) content in both cell types increased significantly (P < 0.05) upon exposure to oxLDL. Conversely, the TC and FC content decreased markedly (P < 0.05) after treatment of cells with rWnt5a. More importantly, both protein and mRNA expression of Caveolin-1 and ATP-binding cassette transporter A1 (ABCA1) was significantly reduced after exposure of wnt5a siRNA-treated cells to oxLDL, whereas rWnt5a treatment of cells resulted in increased Caveolin-1 and ABCA1 protein expression after exposure of cells to oxLDL. Together, these findings demonstrate, for the first time, that Wnt5a reduces the accumulation of cholesterol in lipid-loaded cells by regulating the mRNA expression of Caveolin-1 and ABCA1, which are involved in reverse cholesterol transport. This may present a novel mechanism of Wnt5a-mediated cholesterol transportation in macrophages and VSMC. Therefore, targeting the Wnt5a signalling pathway may have clinical implications in atherosclerosis.

Cell proliferation was inhibited following forced over-expression of miR-30a in the ovary cancer cell line A2780DX5 and the gastric cancer cell line SGC7901R. Interestingly, miR-30a targets the DNA replication protein RPA1, hinders the replication of DNA and induces DNA fragmentation. Furthermore, ataxia telangiectasia mutated (ATM) and checkpoint kinase 2 (CHK2) were phosphorylated after DNA damage, which induced p53 expression, thus triggering the S-phase checkpoint, arresting cell cycle progression and ultimately initiating cancer cell apoptosis. Therefore, forced miR-30a over-expression in cancer cells can be a potential way to inhibit tumour development.

Subjective cognitive decline (SCD) is frequently reported in diabetic patients. Diabetes mellitus (DM) is associated with changes in the microstructure of the brain arise in diabetic patients, including changes in gray matter volume (GMV). However, the underlying mechanisms of changes in GMV in DM patients with cognitive impairment remain uncertain. Here, we present an overview of amyloid‐β‐dependent cognitive impairment in DM patients with SCD. Moreover, we review the evolving insights from studies on the GMV changes in GMV and cognitive dysfunction to which provide the mechanisms of cognitive impairment in T2DM. Ultimately, the novel structural magnetic resonance imaging (MRI) protocol was used for detecting neuroimaging biomarkers that can predict the clinical outcomes in diabetic patients with SCD. A reliable MRI protocol would be helpful to detect neurobiomarkers, and to understand the pathological mechanisms of preclinical cognitive impairment in diabetic patients.

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