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PSMA3 antisense RNA 1 (PSMA3‑AS1), a long noncoding RNA, promotes the progression of esophageal squamous cell carcinoma. However, no study to date has explored the expression or roles of PSMA3‑AS1 in non‑small cell lung carcinoma (NSCLC). The present study examined the expression profile and role of PSMA3‑AS1 in NSCLC. It also aimed to identify how PSMA3‑AS1 promotes the malignant phenotype of NSCLC cells. PSMA3‑AS1 expression in NSCLC tissues and cell lines was measured by reverse transcription‑quantitative polymerase chain reaction. Cell Counting Kit‑8, cell apoptosis, Transwell migration and invasion, and xenograft tumor assays were conducted to study the effects of PSMA3‑AS1 on the aggressive phenotype of NSCLC cells. Furthermore, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, western blotting, and rescue experiments were used to elucidate the interaction among PSMA3‑AS1, microRNA‑409‑3p (miR‑409‑3p), and spindlin 1 (SPIN1) in NSCLC cells. In the present study, high levels ofnotype of NSCLC cells.MicroRNAs (miRNAs) are reported to be involved in renal hypoxia/reoxygenation (H/R) damage. To investigate this further, human kidney (HK‑2) cells were cultured, subjected to H/R and the function of miR‑30a‑5p and glutamate dehydrogenase 1 (GLUD1) was evaluated. The results showed that, miR‑30‑5p was downregulated and GLUD1 was upregulated in HK‑2 cells exposed to H/R. The relationship between miR‑30a‑5p and GLUD1 was determined using dual luciferase assays. Primary HK‑2 cells were cultured in H/R and transfected with negative control 1 (NC1), negative control 2 (NC2), mimic, inhibitor or GLUD1 siRNA plasmids. Reactive oxygen species (ROS) generation, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, and the rate of apoptosis in HK‑2 cells were assessed. The results showed that, miR‑30a‑5p mimic reduced the production of ROS in HK‑2 cells treated with H/R, but increased the activity of SOD, CAT and GPx. In addition, miR‑30a‑5p mimic significantly decreased H/R‑mediated apoptosis, decreased the expression of bax and activity of caspase‑3 and enhanced the expression of bcl‑2. However, miR‑30a‑5p inhibitor showed the opposite effect with regard to the degree of oxidative damage and apoptosis in H/R‑induced HK‑2 cells. Silencing GLUD1 rescued the influence of miR‑30a‑5p inhibitor on oxidative injury and apoptosis in HK‑2 cells stimulated with H/R. These results demonstrated that under H/R conditions, miR‑30a‑5p can reduce oxidative stress in vitro by targeting GLUD1, which may be a novel therapeutic target for liver failure and worth further study.Breast cancer is the most common invasive cancer in women with the highest number of related deaths which is caused by distal metastasis. Recently, integrated analysis of gene expression profile suggested widespread gene dysregulation in various types of cancer. Research in the past decade has focused on long non‑coding RNAs (lncRNAs), particularly in cell proliferation, tumor progression and metastasis. OPA‑interacting protein 5 antisense transcript 1 (OIP5‑AS1) is an evolutionarily conserved long non‑coding RNA that has been linked to oncogenesis in multiple cancers. In breast cancer, dysregulation of OIP5‑AS1 was reported but the precise role in cancer development and progression remains unclear. In the present study, using small interfering RNA (siRNA) targeting OIP5‑AS1, it was shown that knockdown of OIP5‑AS1 was associated with alteration of EMT markers and suppressed migration and invasion of breast cancer cells. Among the EMT‑related transcription factors, ZEB1 and ZEB2 were significantly downregulated with OIP5‑AS1 knockdown. Computational analysis and a dual‑luciferase reporter system identified miR‑340‑5p was the target gene for OIP5‑AS1. Further experiments verified the function of OIP5‑AS1 in cell invasion was dependent on miR‑340a‑5p through regulating target gene ZEB2. In vivo study demonstrated that overexpressing OIP5‑AS1 in breast cancer cells promoted lung metastasis in nude mice. The findings of the present study revealed the mechanism of OIP5‑AS1 in breast cancer metastasis. Overall, our study may provide a potential therapeutic target for breast cancer metastasis.MicroRNA‑590 (miR‑590) has been revealed as a tumor suppressor, while low‑density lipoprotein receptor‑related protein 6 (LRP6) is considered to act as a tumor promoter. PF-03084014 in vivo However, their roles and underlying molecular regulatory mechanisms in esophageal squamous cell carcinoma (ESCC) have yet to be fully elucidated. Therefore, the present study aimed to investigate these mechanisms. The expression levels of miR‑590 and LRP6 in human ESCC samples and cell lines were determined using reverse transcription‑quantitative PCR. Bioinformatics analysis was used to predict the relationship between miR‑590 and LRP6, and luciferase assay was performed to validate the relationship between these factors. Transwell assays were used to determine cell migration and invasion, while western blotting assays were used to detect the protein expression levels of LRP6, E‑cadherin, N‑cadherin and Vimentin. The present study demonstrated that miR‑590 was downregulated and LRP6 was upregulated in ESCC tissues and cell lines. Furthermore, it was found that miR‑590 overexpression and LRP6 knockdown inhibited cell migration, invasion and epithelial‑to‑mesenchymal transition (EMT) in ESCC cell lines. Additional mechanistic studies identified that LRP6 was a target of, and was inhibited by, miR‑590. Collectively, the present findings suggested that miR‑590 inhibited the invasion, migration and EMT of ESCC cells by mediating LRP6.Increasing research has demonstrated that lncRNAs participate in the development of multiple cancer types. However, the role of TTN‑AS1 in endometrial cancer (EC) remains unknown. The present study aimed to explore the function of titin‑antisense RNA1 (TTN‑AS1) in EC progression and the underlying mechanisms. qRT‑PCR was performed to assess the TTN‑AS1 expression patterns in EC tissues and cell lines. Loss of function experiments were carried out to estimate the effects of TTN‑AS1 on EC cell proliferation, migration and invasion. To reveal the underlying mechanisms, informatics tools were used to predict the targets. Rescue experiments were performed to investigate the TTN‑AS1‑regulated miR‑376a‑3p/pumilio homolog 2 (PUM2) axis involved. The results of the present study revealed that TTN‑AS1 was highly expressed in both EC tissues and cell lines, and TTN‑AS1 knockdown inhibited EC cell proliferation, migration and invasion. With respect to the mechanisms, miR‑376a‑3p was revealed to be targeted by TTN‑AS1, and reversed the effects on EC development induced by TTN‑AS1.