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Osteosarcoma is a severe malignant tumor. Several studies indicated that lncRNA prostate cancer‑associated transcript 6 (PCAT6) promoted the development of multiple types of cancers. Studies have also revealed that MDM2 could aggravate tumor symptoms inhibiting P53 expression. However, whether lncRNA PCAT6 could affect the proliferation and metastasis of osteosarcoma cells by regulating P53 expression is unclear. The present study established lncRNA PCAT6‑overexpressing osteosarcoma cells. Cell Counting Kit‑8, wound healing and Transwell assays were performed to detect the change in proliferation, migration and invasion of these cells, respectively. Subsequently, E3 ubiquitin‑protein ligase Mdm2 (MDM2), P53 and P21 expression were determined using western blotting. Finally, MDM2 expression was inhibited and the proliferation, migration and invasion of these cells was determined again. The present study found that the proliferation, migration and invasion of osteosarcoma cells increased following overexpression of lncRNA PCAT6. MDM2 expression was upregulated while the levels of P53 and P21 decreased following overexpression of lncRNA PCAT6. However, the proliferation, migration and invasion of osteosarcoma cells were inhibited following MDM2 knockdown. Additionally, P53 and P21 was rescued following MDM2 knockdown. To conclude, lncRNA PCAT6 promoted the proliferation, migration and invasion of osteosarcoma cells by promoting the expression of MDM2 and suppressing the expression of P53 and P21.Advanced head and neck cancer (HNC) can invade facial bone and cause bone pain, thus posing a significant challenge to the quality of life of patients presenting with advanced HNC. The present study was designed to investigate HNC bone pain (HNC‑BP) in an intratibial mouse xenograft model that utilized an HNC cell line (SAS cells). These mice develop HNC‑BP that is associated with an expression of phosphorylated ERK1/2 (pERK1/2), which is a molecular indicator of neuron excitation in dorsal root ganglia (DRG) sensory neurons. Our experiments demonstrated that the inhibition of high mobility group box 1 (HMGB1) by short hairpin (shRNA) transduction, HMGB1 neutralizing antibody, and HMGB1 receptor antagonist suppressed the HNC‑BP and the pERK1/2 expression in DRG. It was also observed that HNC‑derived HMGB1 increased the expression of the acid‑sensing nociceptor, transient receptor potential vanilloid 1 (TRPV1), which is a major cause of osteoclastic HNC‑BP in DRG. Collectively, our results demonstrated that HMGB1 originating in HNC evokes HNC‑BP via direct HMGB1 signaling and hypersensitization for the acid environment in sensory neurons.Dracocephalum palmatum Stephan (DPS), a medicinal plant used by Russian nomads, has been known to exhibit antioxidant properties. However, to the best of our knowledge, its anticancer effect has not been elucidated. The present study aimed to evaluate the tumor‑suppressive effect of DPS extract (DPSE) in diffuse large B cell lymphoma (DLBCL) and the underlying mechanism. MTS assays and Annexin V staining were performed to assess the anti‑proliferative and apoptotic effects of DPSE, respectively. To reveal the underlying mechanisms, the levels of pro‑ and anti‑apoptotic Bcl‑2 members were analyzed by western blotting. Rescue experiments were performed to investigate the potential involvement of Myc in DPSE‑induced tumor‑inhibitory effects. Additionally, high‑performance liquid chromatography analysis was performed to analyze the components with anticancer effects. Exposure of multiple DLBCL cell lines to DPSE significantly decreased cell viability and increased apoptosis, whereas it had no effect on the survivvestigation of the fraction with bioactive compounds demonstrated that flavonoids may be responsible for most, if not all, of the anti‑lymphoma effect. Efforts to identify the bioactive flavonoids is currently underway.Among all types of kidney diseases, renal cell carcinoma (RCC) has the highest mortality, recurrence and metastasis rates, which results in high numbers of tumor‑associated mortalities in China. Identifying a novel therapeutic target has attracted increasing attention. Bromodomain and extraterminal domain (BET) proteins have the ability to read the epigenome, leading to regulation of gene transcription. As an important member of the BET family, bromodomain testis‑specific protein (BRDT) has been well studied; however, the mechanism underlying BRDT in the regulation of RCC has not been fully investigated. Eukaryotic translation initiation factor 4E‑binding protein 1 (eIF4EBP1) is a binding partner of eIF4E that is involved in affecting the progression of various cancer types via regulating gene transcription. To identify novel regulators of eIF4EBP1, an immunoprecipitation assay and mass spectrometry analysis was performed in RCC cells. It was revealed that eIF4EBP1 interacted with BRDT, a novel interacting pr or BRDT knockdown suppressed the growth of RCC via decreasing eIF4EBP1, thereby leading to decreased c‑myc transcription levels. https://www.selleckchem.com/products/filgotinib.html Considering the regulatory function of BET proteins in gene transcription, the present study suggested that there is a novel mechanism underlying eIF4EBP1 regulation by BRDT, and subsequently decreased c‑myc in RCC, and further identified a new approach by regulating eIF4EBP1 or c‑myc for enhancing BRDT‑targeting RCC therapy.MicroRNA‑7 (miR‑7) has been identified as a tumor suppressor in non‑small cell lung cancer (NSCLC) and a radiosensitivity regulator. Numerous studies have revealed that specific protein 1 (SP1) plays a critical role in the tumorigenesis of various types of cancers and regulates radiosensitivity and tumor suppressor p53‑binding protein 1 (TP53BP1), which plays an essential role in DNA repair. However, it is not clear whether miR‑7 has a regulatory effect on SP1 and TP53BP1 in NSCLC. In the present study it was revealed that miR‑7 directly binds to the 3'UTR of SP1, thereby suppressing SP1 expression to regulate radiosensitivity. Overexpression of miR‑7 and SP1 and knockdown of miR‑7 and SP1 were performed using lentiviral transfection. Protein and mRNA abundance of SP1 and TP53BP1 were determined using western blotting and RT‑qPCR, respectively, while miR‑7 binding to SP1 was validated using a luciferase reporter assay. Biological function analysis indicated that miR‑7 negatively regulated SP1 and inhibited cell proliferation, migration, and invasion when combined with radiation.