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Immunohistochemistry revealed that SLP‑2 was increased in liver metastatic sites. Microarray analysis indicated that this protein regulated the expression of glutamine‑fructose‑6‑phosphate transaminase 2 (GFPT2), a rate‑limiting enzyme of the hexosamine biosynthesis pathway. SLP‑2 contributed to the malignant character of PC by inducing liver metastasis. Cell motility and glucose uptake may be induced via the hexosamine biosynthesis pathway through the expression of GFPT2. The present study revealed a new mechanism of liver metastasis and indicated that SLP‑2 and its downstream pathway could provide novel therapeutic targets for PC.Lung cancer is the leading cause of cancer‑associated death worldwide and exhibits intrinsic and acquired therapeutic resistance to cisplatin (CIS). The present study investigated the role of mTOR signaling and other signaling pathways after metformin (MET) treatment in control and cisplatin‑resistant A549 cells, mapping pathways and possible targets involved in CIS sensitivity. MTT, flow cytometry, clonogenic assay, western blotting, proteomic analysis using the Stable Isotope Labeling by Amino acids in Cell culture (SILAC) approach and reverse transcription‑quantitative PCR were performed. The results revealed that CIS treatment induced mTOR signaling pathway overactivation, and the mTOR status was restored by MET. MET and the mTOR inhibitor rapamycin (RAPA) decreased the viability in control and resistant cells, and decreased the cell size increase induced by CIS. In control cells, MET and RAPA decreased colony formation after 72 h and decreased IC50 values, potentiating the effects of CIS. Proteomics analysis revealed important pathways regulated by MET, including transcription, RNA processing and IL‑12‑mediated signaling. In CIS‑resistant cells, MET regulated the apoptotic process, oxidative stress and G2/M transition. Annexin 4 (ANXA4) and superoxide dismutase 2 (SOD2), involved in apoptosis and oxidative stress, respectively, were chosen to validate the SILAC analysis and may represent potential therapeutic targets for lung cancer treatment. In conclusion, the chemosensitizing and antiproliferative effects of MET were associated with mTOR signaling and with potential novel targets, such as ANXA4 and SOD2, in human lung cancer cells.Spinal cord injury (SCI) is one of the most debilitating of all the traumatic conditions that afflict individuals. For a number of years, extensive studies have been conducted to clarify the molecular mechanisms of SCI. Experimental and clinical studies have indicated that two phases, primary damage and secondary damage, are involved in SCI. The initial mechanical damage is caused by local impairment of the spinal cord. In addition, the fundamental mechanisms are associated with hyperflexion, hyperextension, axial loading and rotation. By contrast, secondary injury mechanisms are led by systemic and cellular factors, which may also be initiated by the primary injury. Although significant advances in supportive care have improved clinical outcomes in recent years, a number of studies continue to explore specific pharmacological therapies to minimize SCI. FLT3-IN-3 The present review summarized some important pathophysiologic mechanisms that are involved in SCI and focused on several pharmacological and non‑pharmacological therapies, which have either been previously investigated or have a potential in the management of this debilitating injury in the near future.Prion diseases, which involve the alteration of cellular prion protein into a misfolded isoform, disrupt the central nervous systems of humans and animals alike. Prior research has suggested that peroxisome proliferator‑activator receptor (PPAR)γ and autophagy provide some protection against neurodegeneration. PPARs are critical to lipid metabolism regulation and autophagy is one of the main cellular mechanisms by which cell function and homeostasis is maintained. The present study examined the effect of troglitazone, a PPARγ agonist, on autophagy flux in a prion peptide (PrP) (106‑126)‑mediated neurodegeneration model. Western blot analysis confirmed that treatment with troglitazone increased LC3‑II and p62 protein expression, whereas an excessive increase in autophagosomes was verified by transmission electron microscopy. Troglitazone weakened PrP (106‑126)‑mediated neurotoxicity via PPARγ activation and autophagy flux inhibition. A PPARγ antagonist blocked PPARγ activation as well as the neuroprotective effects induced by troglitazone treatment, indicating that PPARγ deactivation impaired troglitazone‑mediated protective effects. In conclusion, the present study demonstrated that troglitazone protected primary neuronal cells against PrP (106‑126)‑induced neuronal cell death by inhibiting autophagic flux and activating PPARγ signals. These results suggested that troglitazone may be a useful therapeutic agent for the treatment of neurodegenerative disorders and prion diseases.The aim of the present study was to observe the temporal changes in the chest based on findings from imaging in severe patients with novel coronavirus pneumonia. A total of 33 severe confirmed cases (20 male patients and 13 female patients) were enrolled in the present study between January 31, 2020 and March 10, 2020. Chest imaging findings and clinical data were collected and analyzed. The median age was 65 years (age range, 25‑90 years). As of April 7, 2020, 24 patients were discharged, and 9 patients died. With regards to the clinical manifestations, 28 patients had fever, 17 patients had a cough and 15 patients had shortness of breath. Of these, 29 patients had underlying health conditions. Ground glass opacities, consolidation and interlobular septal thickening were the most common and typical chest computerized tomography (CT) scan abnormalities. A total of 6/33 (18.2%) patients had 1 affected lobe, 6/33 (18.2%) patients had 2 affected lobes, 5/33 (15.2%) patients had 3 affected lobes, 9/33 (27.3%) patients had 4 affected lobes and 7/33 (21.2%) patients had 5 affected lobes in the initial chest CT scan. The mean interval time between two consecutive CT examinations was 4.5 days (range, 3‑9 days). Most severe patients exhibited some degree of aggravation based on the CT findings in the 3 weeks from illness onset. After 3 weeks from illness onset, these severe survivors demonstrated improvements in the chest CT findings, which included complete absorption or only a few remaining fibrous stripes. Chest CT manifestations of patients infected with novel coronavirus pneumonia were diverse and varied. Severe patients had imaging features of rapid progression and slow absorption. Monitoring of chest imaging findings is vital to detect any changes in a timely manner.FLT3-IN-3