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In addition, astrocyte activation was markedly suppressed by β‑Lapachone‑cotreatment with L‑DOPA in the striatum and substantia nigra of the unilateral 6‑OHDA model. These findings suggest that β‑Lapachone cotreatment with L‑DOPA therapy may have therapeutic potential for the suppression or management of the development of L‑DOPA‑induced dyskinesia in patients with PD.The aim of the present study was to explore the effect of microRNA (miR)‑153 on the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) in a hypoxic condition by targeting ρ‑associated, coiled‑coil‑containing protein kinase 1 (ROCK1) and nuclear factor of activated T cells cytoplasmic 3 (NFATc3). The right ventricular systolic pressure, right ventricular hypertrophy index, medial wall thickness and medial wall area were studied at different time‑points after rats were exposed to hypoxia. Western blot analysis was used to detect ROCK1 and NFATc3 protein levels. In addition, reverse transcription‑quantitative (RT‑q) PCR was performed to confirm the mRNA levels of miR‑153, ROCK1 and NFATc3 in human (H)PASMCs under hypoxic conditions. Transfected cells were then used to evaluate the effect of miR‑153 on cell proliferation and migration abilities. The association between miR‑153 and ROCK1 or NFATc3 was identified through double luciferase assays. Hypoxia induced pulmonary vascular remodeling and pulmonary arterial hypertension, which resulted from the abnormal proliferation of HPASMCs. ROCK1 and NFATc3 were the target genes of miR‑153 and miR‑153 mimic inhibited the protein expressions of ROCK1 and NFATc3 in HPASMCs and further inhibited cell proliferation and migration under hypoxic conditions. By contrast, the miR‑153 inhibitor promoted the proliferation and migration of HPASMCs. miR‑153 regulated the proliferation and migration of HPASMCs under hypoxia by targeting ROCK1 and NFATc3.Lung cancer is one of the most common types of cancer and has a high mortality rate, worldwide. The major histopathological subtype is non‑small cell lung cancer (NSCLC). The aim of the present study was to investigate the role of long non‑coding (lnc) RNA PITPNA antisense RNA 1 (PITPNA‑AS1) in NSCLC and elucidate its potential mechanisms. The expression of PITPNA‑AS1 was determined in several NSCLC cell lines. Following PITPNA‑AS1‑silencing, cell proliferation, invasion and migration were evaluated using Cell Counting Kit‑8, colony formation, Transwell assay and wound healing assays, respectively. The expression levels of proliferation‑, migration‑ and epithelial‑mesenchymal transition (EMT)‑associated proteins were examined using immunofluorescence assay or western blot analysis. A luciferase reporter assay was conducted to verify the potential interaction between PITPNA‑AS1 and microRNA(miR)‑32‑5p. Subsequently, rescue assays were performed to investigate the effects of PITPNA‑AS1 and miR‑32‑5p on NSCLC progression. The results demonstrated that PITPNA‑AS1 was highly expressed in NSCLC tissues and cell lines. It was found that PITPNA‑AS1 silencing inhibited the proliferation, invasion and migration of NSCLC cells. Furthermore, the protein expression of E‑cadherin was upregulated, while the expression levels N‑cadherin and vimentin were downregulated. Tanespimycin The luciferase reporter assay confirmed that miR‑32‑5p was a direct target of PITPNA‑AS1. The rescue experiments suggested that a miR‑32‑5p inhibitor significantly reversed the inhibitory effects of PITPNA‑AS1 silencing on proliferation, invasion, migration and EMT in NSCLC cells. Collectively, the present results demonstrated that PITPNA‑AS1 silencing could suppress the progression of NSCLC by targeting miR‑32‑5p, suggesting a promising biomarker in NSCLC diagnosis and treatment.Prostate cancer (PCa) is a leading cause for death in men and the most commonly diagnosed malignancy globally. MicroRNA (miR)‑583 expression levels have been discovered to be downregulated in recurrent PCa samples compared with non‑recurrent cases. However, the precise functions and pathogenic mechanism of miR‑583 in the development of PCa are vague, thus the aim of the present study was to investigate these. The expression levels of miR‑583 and Janus kinase 1 (JAK1) in PCa tissues and cell lines were analyzed using reverse transcription‑quantitative PCR and western blotting. The protein expression levels of phosphorylated (p)‑STAT3 and STAT3 in PCa cell lines were also analyzed using western blotting. The effects of miR‑583 and JAK1 on the proliferation and invasion of PCa cell lines cell lines were determined using MTT and Transwell assays, respectively. The binding interaction between miR‑583 and the 3'‑untranslated region of JAK1 were predicted by TargetScan, and further validated using dual luciferase reporter assays in PCa cell lines. The results revealed that the expression levels of miR‑583 were downregulated, while those of JAK1 were upregulated in PCa tissues and cell lines (DU145 and PC3). The transfection with the miR‑583 mimic inhibited the proliferation and invasion, as well as downregulating JAK1 and p‑STAT3 protein expression levels in DU145 and PC3 cell lines. These effects were partially abolished following the overexpression of JAK1. Moreover, JAK1 was identified to be a target gene for miR‑583 in DU145 and PC3 cell lines and the expression levels of miR‑583 were revealed to be negatively correlated with JAK1 expression levels in PCa tissues. In conclusion, the findings of the present study suggested that miR‑583 may inhibit the proliferation and invasion of PCa cells by targeting JAK1, thus providing a novel therapeutic target for patients with PCa.Osteoarthritis (OA) is the most prevalent joint disorder characterized by progressive cartilage damage, resulting in gradual disability among the elderly. We previously provided in vivo evidence that nuclear factor erythroid 2‑related factor 2 (Nrf2) deficiency is associated with the development of OA. It has been reported that coniferaldehyde (CFA) acts as a potential Nrf2 activator. The aim of the present study was to investigate the protective effects of CFA against osteoarthritis. A murine model of surgical‑induced OA was used in the present study and CFA was administered by peritoneal injection every day, and the knee joints were assessed by histological analysis. The results demonstrated that CFA activated the Nrf2 signaling pathway in primary chondrocytes and articular cartilage from the knee joints. Cartilage damage in mice subjected to the destabilization of the medial meniscus was evidently alleviated by CFA treatment. CFA also robustly suppressed apoptosis induced by H2O2 in murine chondrocytes and reduced the expression of matrix metalloproteinase (MMP)1, MMP3, interleukin (IL)‑1 and IL‑6 in vivo.