Lammmoran9182

Retinoblastoma (RB) is an intraocular malignancy that mainly affects young children. Previous reports have demonstrated that mutations or the inactivation of the RB1 gene were the main cause of RB; however, disruption of the intracellular signaling pathways following deficiency of RB1 requires further investigation. Based on the Gene Expression Omnibus data and bioinformatics prediction, the present study aimed to investigate the microRNA (miR)‑338‑3p/neuro‑oncological ventral antigen 1 (NOVA1) axis in RB. Subsequently, overexpression and knockdown of miR‑338‑3p and NOVA1, respectively, were performed to study the role of miR‑338‑3p/NOVA1 in the progression of the RB cells. The results demonstrated that overexpression of miR‑338‑3p significantly inhibited cell proliferation, migration and invasion, and promoted apoptosis of the RB cells. Moreover, knockdown of NOVA1 showed similar results. A dual‑luciferase reporter assay and rescue experiments further confirmed the direct binding between miR‑338‑3p and NOVA1. Taken together, the results indicated that miR‑338‑3p acted as tumor suppressor by targeting the oncogene of NOVA1 in RB, which may serve as potential therapeutic targets in RB.Hepatocellular carcinoma (HCC) is one of the most aggressive types of malignancy worldwide. However, the mechanism underlying its frequent recurrence remains unclear. Studies have demonstrated that spindle and kinetochore associated complex subunit 3 (SKA3) is highly expressed in colorectal and prostate cancer. The present study aimed to determine whether SKA3 could be a predictive and prognostic marker for liver cancer. SKA3 expression levels in liver cancer cell lines, liver cancer tissues, normal liver cells and non‑cancerous tissues were compared at both transcriptional and translational levels. Correlation between SKA3 levels, clinicopathological characteristics and patient survival was also assessed. Gene set enrichment analysis (GSEA) was performed to identify SKA3‑associated pathways. Furthermore, SKA3 was knocked down and overexpressed in liver cancer cells, and then assessed the effect on cell proliferation, cell cycle, and tumor formation ability. Kaplan‑Meier survival analysis and log‑rank test wee a promising prognostic biomarker and candidate for targeted therapy.Recent studies have reported the important roles of dopamine receptors in the early development and progression of glioblastoma (GBM). The present research aimed to explore the antineoplastic effect and intrinsic pathways of action of dopamine receptor D1 agonist SKF83959 on GBM cells. Flow cytometric analysis revealed a significant level of apoptotic cell death under SKF83959 treatment. SKF83959 administration increased intracellular calcium levels and oxidative stress through the phospholipase C/inositol trisphosphate pathway. The downstream calpains were activated and dysregulated by the increased calcium levels. The mitochondrial membrane potential‑dependent staining assay revealed decreased mitochondrial transmembrane potential in GBM cells under SKF83959 treatment. The mitochondrial/cytosolic fraction and western blotting further demonstrated mitochondrial dysfunction and endoplasmic reticulum stress, followed by apoptosis. The calpain inhibitor, calpastatin, significantly reversed the increase in mitochondrial injury and endoplasmic reticulum stress and eventually ameliorated GBM cell apoptosis during SKF83959 treatment. Finally, the in vivo inhibitory efficacy of SKF83959 was verified in GBM xenograft models. In addition, immunohistochemistry and western blotting both revealed increased expression of calpains in xenograft GBM tissues. These results suggested a potential therapeutic target for human GBM treatment regarding calpain expression and activity regulation.Cisplatin (DDP)‑based chemotherapy is a standard treatment for cervical cancer, although chemotherapy resistance remains a major concern. Hypoxia‑inducible factor‑2 α (HIF‑2α) plays an important role in chemotherapy resistance. MicroRNAs (miRs) can inhibit gene expression by binding to the 3'‑untranslated region of the target gene. The authors' previous study showed that miR‑519d‑3p plays an important role in the regulation of HIF‑2α expression under hypoxic conditions in cervical cancer. However, the function and regulatory mechanisms of the miR‑519d‑3p/HIF‑2α axis in DDP‑resistance in cervical cancer are not fully understood. Therefore, the aim of the present study was to investigate whether the miR‑519d‑3p/HIF‑2α axis increased DDP resistance by regulating the PI3K/AKT signaling pathway. It was found that the expression of miR‑519d‑3p was lower in DDP‑resistant cervical cancer cells (CaSki/DDP and HeLa/DDP) compared with CaSki and HeLa cells under hypoxic conditions. Additionally, miR‑519d‑3p overexpression decreased the IC50 value in CaSki/DDP and HeLa/DDP cells, and inhibited HIF‑2α protein expression and the PI3K/AKT signaling pathway under hypoxic conditions. Furthermore, it was demonstrated that HIF‑2α overexpression reduced the effect of miR‑519d‑3p overexpression on HeLa/DDP and CaSki/DDP cells. Moreover, the present results suggested that HIF‑2α overexpression increased the IC50 value in CaSki/DDP and HeLa/DDP cells. It was also found that HIF‑2α overexpression reduced the effect of miR‑519d‑3p overexpression on the PI3K/AKT signaling pathway. Therefore, the present results indicated that the miR‑519d‑3p/HIF‑2α axis increased DDP resistance of cervical cancer cells by suppressing the PI3K/AKT signaling pathway under hypoxic conditions.Immunogene therapy can enhance the antitumor immune effect by introducing genes encoding co‑stimulation molecules, cytokines, chemokines and tumor‑associated antigens into treatment cells or human cells through genetic engineering techniques. see more Oncolytic viruses can specifically target tumor cells and replicate indefinitely until they kill tumor cells. If combined with immunogene therapy, oncolytic viruses can play a more powerful antitumor role. The high pressure, hypoxia and acidity in the tumor microenvironment (TME) provide suitable conditions for tumor cells to survive. To maximize the potency of oncolytic viruses, various methods are being developed to promote the reversal of the TME, thereby maximizing transmission of replication and immunogenicity. The aim of the present review was to discuss the basic mechanisms underlying the effects of oncolytic adenoviruses on the TME, and suggest how to combine the modification of the adenovirus with the TME to further combat malignant tumors.