Natural products are a great source of cancer chemotherapeutic agents. The present study was conducted to investigate whether cucurbitacin B (CuB), one of the most potent and widely used cucurbitacins, inhibits proliferation and induces apoptosis in the A549 lung cancer cell line. Furthermore, CuB induced apoptosis of A549 cells in a concentration-dependent manner, as determined by fluorescence microscopy, flow cytometry and transmission electron microscopy. The present study also demonstrated that CuB dose-dependently inhibited lung cancer cell proliferation, with cell cycle inhibition and cyclin B1 downregulation. Apoptosis induced by CuB was shown to be associated with cytochrome c release, B-cell lymphoma 2 downregulation and signal transducer and activator of transcription 3 pathway inhibition. CuB may prove to be a useful approach for the chemotherapy of lung cancer.
MicroRNAs (miRNAs) are a class of endogenous, non-coding, single-stranded RNAs with a length of approximately 22 nucleotides that are found in eukaryotes. miRNAs are involved in the regulation of cell differentiation, proliferation, invasion, apoptosis, and metabolism by regulating the expression of their target genes. Emerging studies have suggested that various miRNAs play key roles in the pathogenesis of central nervous system (CNS) disorders and may be viable therapeutic targets. In particular, miR-21 has prominently emerged as a focus of increasing research on the mechanisms of its involvement in CNS disorders. Herein, we reviewed recent studies on the critical roles of miR-21, including its dysregulated expression and target genes, in the regulation of pathophysiological processes of CNS disorders, with a special focus on apoptosis and inflammation. Collectively, miR-21 is a versatile regulator in the progression of CNS disorders and could be a promising biomarker and therapeutic target for these diseases. An in-depth understanding of the mechanisms by which miR-21 affects the pathogenesis of CNS disorders could pave the way for miR-21 to serve as a therapeutic target for these conditions.
Alzheimer’s disease (AD) is a common neurodegenerative disease in the elderly and is the most common type of dementia. AD is mostly gradual onset, and involves slow, progressive mental decline, accompanied by personality changes; the incidence of AD gradually increases with age. The etiology of AD is unknown, although it is currently believed to be related to abnormal deposition of amyloid β-protein (Aβ) in the brain, hyperphosphorylation of microtubule-associated protein tau, and the release of various cytokines, complements, activators and chemokines by cells. MicroRNAs (miRNAs) are a class of highly conserved non-coding RNAs that regulate gene expression at the post-transcriptional level, and manipulate the functions of intracellular proteins and physiological processes. Emerging studies have shown that miRNA plays an important role in regulating AD-related genes. MiR-132 is known as “NeurimmiR” due to its involvement in numerous neurophysiological and pathological processes. Accumulating pre-clinical results suggest that miR-132 may be involved in the progression of Aβ and tau pathology. Moreover, clinical studies have indicated that decreased circulating miR-132 levels could be used a potential diagnostic biomarker in AD. Here, we review the pathogenic role of miR-132 activity in AD, and the potential of targeting miR-132 for developing future therapeutic strategies.
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