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Evidence suggests that both 14-3-3κ and long non-coding RNA HOX transcript antisense RNA (HOTAIR) are involved in the tumorigenesis and progression of lung cancer. In the present study, the potential association between 14-3-3κ and HOTAIR in non-small cell lung cancer (NSCLC) was investigated. In tissue samples collected from 54 patients with NSCLC, expression of HOTAIR and 14-3-3κ was analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). After stable ectopic expression of HOTAIR and stable HOTAIR knockdown in PC9 cancer cells, the effect of HOTAIR on levels of mRNA and protein 14-3-3κ expression levels were detected using RT-qPCR and western blotting, respectively. Expression of HOTAIR and 14-3-3κ in NSCLC tissues was significantly higher than in adjacent non-cancerous lung tissue (P<0.05). Correlation analysis also identified a correlation between levels of HOTAIR and 14-3-3κ expression in NSCLC tissues (r=0.725, P=0.0005). In addition, overexpression and knockdown of HOTAIR in the human NSCLC cell line PC9 led to the upregulation and downregulation of 14-3-3κ, respectively, at both the mRNA and protein levels (all P<0.05). To the best of our knowledge, the present study provides the first in vivo and in vitro evidence to suggest that HOTAIR promotes the expression of 14-3-3κ in NSCLC. The potential association between HOTAIR and 14-3-3κ indicates that both biomolecules may be viable targets in anticancer therapy. [ABSTRACT FROM AUTHOR]

The discovery of cell‑free DNA fetal (cff DNA) in maternal plasma during pregnancy provides a novel perspective for the development of non‑invasive prenatal diagnosis (NIPD). Against the background of maternal DNA, the use of the relatively low concentration of cff DNA is limited in NIPD. Therefore, in order to overcome the complication of the background of maternal DNA and expand the scope of cff DNA application in clinical practice, it is necessary to identify novel universal fetal‑specific DNA markers. The GeneChip Human Promoter 1.0R Array set was used in the present study to analyze the methylation status of 12 placental tissue and maternal peripheral blood whole‑genome DNA samples. In total, 5 fetus differential hypermethylation regions and 6 fetus differential hypomethylation regions were identified. In order to verify the 11 selected methylation regions and detect the differential CpG sites in these regions, a bisulfate direct sequencing strategy was used. In total, 87 fetal differential methylation CpG sites were identified from 123 CpG sites. The detection of fetal differential methylation DNA regions and CpG sites may be instrumental in the development of efficient NIPD and in the expansion of its application in other disorders. [ABSTRACT FROM AUTHOR]

Doxorubicin (DOX) is one of the most effective chemotherapeutic drugs. However, its clinical use has been hampered due to the development of cardiotoxicity. Vitexin, which is the active ingredient of hawthorn leaf extract, has various biological activities, including antioxidant and anti-inflammatory actions. The present study aimed to investigate whether vitexin was able to protect against DOX-induced acute cardiotoxicity in model rats and the mechanisms of this protective effect were assessed. Adult Sprague-Dawley rats were randomly assigned into the control (saline only), model (DOX only) and vitexin-treated (DOX plus vitexin) groups. Rats in the model and vitexin-treated groups were injected with DOX (2 mg/kg; i.p.) once a week for 4 weeks. Rats in the vitexin-treated group were administered 30 mg/kg oral vitexin once daily at doses for 4 weeks. The levels of lactate dehydrogenase, creatine kinase isoenzyme-MB, malondialdehyde, superoxide dismutase, catalase and myeloperoxidase were assessed using assay kits. The levels of inflammatory mediators, including tumor necrosis factor-α, interleukin (IL)-1β, IL-6, nuclear factor (NF)-κB, and caspase-3, were assayed by the enzyme-linked immunosorbent assay method. Western blot analysis was performed to assess the protein expression levels of p-FOXO3a. Vitexin pretreatment significantly protected against DOX-induced myocardial damage, which was characterized by increased serum creatine kinase isoenzyme-MB and lactate dehydrogenase. Vitexin significantly ameliorated oxidative stress injury evoked by DOX, demonstrated by the inhibition of lipid peroxidation and the elevation of antioxidant enzyme activities. Furthermore, DOX provoked inflammatory responses by increasing the expression levels of IL-1β, IL-6, NF-κB and tumor necrosis factor-α, whereas vitexin pretreatment significantly inhibited these inflammatory responses. Notably, DOX induced apoptotic tissue damage by increasing caspase-3 activity, whereas vitexin administration was able to decrease caspase-3 activity. In addition, vitexin induced elevated FOXO3a protein expression levels in the vitexin-treated group. In conclusion, the findings of the present study suggested that vitexin possesses cardioprotective action against DOX-induced cardiotoxicity by suppressing oxidative stress, inflammation and apoptotic signals. [ABSTRACT FROM AUTHOR]

In the present study, the alterations in uncoupling protein 2 (UCP2) expression following hypothermic preservation in rat hearts were investigated. Isolated rat hearts were preserved in Celsior solution for 3-12 h followed by 60 min of reperfusion. The cardiac function was evaluated using the Langendorff perfusion system. UCP2 and silent mating type information regulation 2 homolog 1 (SIRT1) proteins were detected by western blot analysis. The ATP production and mitochondrial reactive oxygen species (ROS) levels were assessed. Subsequent to preservation in ice-cold Celsior solution for 3-12 h, the UCP2 protein expression in rat hearts was observed to increase in a time-dependent manner. The UCP2 inhibitor genipin inhibited the hypothermic preservation- induced cardiac dysfunction, prevented a decline in ATP production induced by 9 h of preservation, however had no effect on the hypothermic preservation-induced increase in mitochondrial ROS levels. Compared with the control group, the SIRT1 protein expression in rat hearts reduced following hypothermic preservation. Compared with the 9-h preservation group, Celsior solution supplemented with the SIRT1 activator resveratrol (20 or 40 µmol/l) inhibited UCP2 protein overexpression, prevented the decline in ATP production and resulted in an improvement cardiac function. The SIRT1 inhibitor EX-527 abolished the resveratrol-induced inhibition of UCP2 overexpression and cardiac protection in the hypothermic preserved rat heart. These observations suggest that downregulation of UCP2 expression in the hypothermic preserved rat heart in part initiated the protective mechanism via the SIRT1 pathway. [ABSTRACT FROM AUTHOR]

Pure yolk sac tumors are extremely rare in adults; to the best of our knowledge, <20 cases have been reported. Multiple metastases originating from a pure yolk sac testicular tumor, descending from an intra-abdominal testis, are additionally extremely rare. In the present case, a man exhibiting a 30-year history of cryptorchidism and indirect inguinal hernia, was admitted to the Department of Urology (The Second Xiangya Hospital, Changsha, China) due to a mass that had descended from the abdominal cavity 7 months previously. Elevated levels of specific serum marker (α-fetoprotein, lactate dehydrogenase and human chorionic gonadotropin) did not indicate potential testicular germ cell types prior to surgery and pathological examination. Pathological results and immunohistochemistry revealed a testicular pure yolk sac tumor subsequent to surgery. The present case report and literature review describes the typical characteristics of an adult testicular yolk sac tumor, as well as the diagnosis and management of the disease. [ABSTRACT FROM AUTHOR]

Metadherin (MTDH), also known as astrocyte-elevated gene-1, was first cloned in 2002 and has been confirmed as an oncogene in numerous types of cancer by previous studies. Overexpression of MTDH has been observed in multiple types of cancer, including breast, esophageal, prostate, cervical and non-small-cell lung cancer, as well as neuroblastoma and hepatocellular carcinoma. However, at present, few investigations into MTDH-associated prostate cancer have been performed. A previous study suggested that MTDH was expressed at higher levels in prostate cancer samples, compared with those of benign prostatic hyperplasia. The present study aimed to elucidate the effects of MTDH as an oncogene associated with the biological behavior of prostate cancer cells and chemotherapy-sensitivity to cisplatin in vitro. It was demonstrated that the inhibition of MTDH expression promoted cell apoptosis, reduced cell viability and weakened the invasive ability of prostate cancer cells. In addition, the suppression of MTDH expression increased cell sensitivity to cisplatin. Furthermore, it was demonstrated that MTDH-associated phosphoinositide 3-kinase/Akt signaling pathways may be involved in mediating the biological behavior of prostate cancer. [ABSTRACT FROM AUTHOR]

Myocardial dysfunction in sepsis is associated with an increased risk of mortality. The mitochondrial aldehyde dehydrogenase (ALDH2) enzyme is crucial for protecting the heart from ischemic injury. The aim of the present study was to determine the role of ALDH2 in cardiac dysfunction induced by lipopolysaccharide (LPS). Male rats were treated intraperitoneally with LPS, and their stroke volume and cardiac output were evaluated using an M-mode echocardiograph. The expression levels and activity of ALDH2, nitric oxide content and inducible nitric oxide synthase (iNOS) activity, and the opening of the mitochondrial permeability transition pore (MPTP) were also evaluated. Treatment with LPS (5, 10, or 20 mg/kg) resulted in a steady decrease in cardiac output and stroke volume. The ALDH2 activity was decreased in a dose-dependent manner; however, the ALDH2 protein expression levels remained unchanged. Alda-1, a specific activator of ALDH2, increased the activity of ALDH2 and lessened LPS-induced cardiac dysfunction. A marked opening of the MPTP was observed 12 h following treatment with LPS, which was prevented by Alda-1. The improvement in cardiac function in response to treatment with Alda-1, was partially prevented by treatment with the MPTP inhibitor atractyloside. LPS treatment induced an increase in iNOS activation and inhibition of ALDH2 activity. The iNOS selective inhibitor, aminoguanidine, partially reversed the LPS-induced ALDH2 activity decrease and MPTP opening. These results indicate that ALDH2 activity may have a role in protecting against LPS-induced cardiac dysfunction. The potential mechanism may involve inhibition of MPTP opening and iNOS expression. [ABSTRACT FROM AUTHOR]

Metadherin (MTDH) has been identified as an important oncogene in carcinogenesis, tumor progression and metastasis in numerous malignancies, through signal transduction pathways. MTDH is a potential biomarker and therapeutic target in cancers. The present systematic review was performed to search for studies regarding MTDH and prostate, bladder and kidney cancer using several databases and the eligible studies were reviewed. MTDH expression was found to significantly increase in prostate, bladder and kidney cancers, not only in clinical tissue samples, but also in cancer cell lines. Reviewing the clinical and statistical analysis revealed that MTDH may be involved in urologic cancer progression, metastasis and prognosis. MTDH may be an independent or one of the cofactors in urologic cancers for prediction of patient survival, and may be involved in potential anticancer strategies. MTDH may be associated with several signal transduction pathways in urologic cancers, indicating latent targets to develop anticancer therapeutic strategy. Further studies are required to confirm these findings. [ABSTRACT FROM AUTHOR]

Eosinophilia is typically associated with allergic reactions, parasitic infestations, certain forms of vasculitis, the use of certain medications and hematologic malignancies. In addition to eosinophilia associated with gastrointestinal tumors, lung cancer and thyroid carcinoma in solid malignancies, there are a limited number of cases describing peripheral hypereosinophilia in urologic tumors. The present study reports three cases of eosinophilia in patients with chromophobe renal cell carcinoma (CRCC) and investigates the association between excessive eosinophilia and the recurrence and prognosis of renal carcinoma. This is the first report of CRCC associated with excessive eosinophilia. Eosinophilia following tumor resectioning may indicate a poor prognosis, tumor recurrence and rapid disease progression. [ABSTRACT FROM AUTHOR]

Primary kidney parenchyma squamous cell carcinoma is extremely rare, and this is the forth case to be reported. In the present study, a case of a 61-year old man is discussed. The man presented with recurrent lumbago, gross hematuria for nearly 2 months, and suspicious inflammatory kidney diseases on contrast-enhanced computed tomography (CT) and fludeoxyglucose-positron emission tomography (FDG-PET)/CT, but a tumor can not be excluded completely prior to surgery. Finally, radical nephrectomy was performed, and histological analysis determined that the diagnosis was kidney parenchyma squamous cell carcinoma with inflammation invasion. The present case highlights the potential confusion of preoperative diagnosis of renal tumor with inflammation, and introduces the potential role of FDG-PET in its diagnosis and survival evaluation in renal malignancies. [ABSTRACT FROM AUTHOR]