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Objective: Papillary thyroid cancer (PTC) is one of the most common thyroid cancers and its prevalence has increased in recent years. Studies have shown that autophagy, angiogenesis, inflammation, oxidative damage, apoptosis, and some signaling pathways such as PI3K/AKT/mTOR play an important role in cancer progression. Moreover, most of their signaling molecules are the clients of heat shock protein 90 (HSP90), and its inhibition attenuates tumorigenesis. Diphenyl difluoroketone (EF-24), a curcumin analog, has antioxidative, anti-inflammatory, and anticancer properties and, unlike curcumin, has high efficacy, and may treat PTC. Therefore, the antioxidant, anti-inflammatory, angiogenic, apoptotic, and anticancer effects of EF-24 on PTC cell lines (BCPAP and TPC-1) were investigated in this study. Methods: In this study, the effect of different concentrations of EF-24 and cisplatin on cell viability, apoptosis, inflammation, autophagy, oxidative status, and angiogenesis, along with HSP90 expression was evaluated in BCPAP and TPC-1 cell lines. Results: The results showed that treatment with different EF-24 concentrations could significantly decrease cell viability by inducing apoptosis. EF-24 (40 µg/mL) also significantly downregulated HSP90 and the gene and protein involved in oxidative damage, angiogenesis, inflammation, and autophagy. Conclusions: In conclusion, EF-24 could decrease cell viability by inducing apoptosis mediated by autophagy, oxidative stress, angiogenesis, inflammation, and the PI3K/ AKT/mTOR pathway. It is possible that a decrease in HSP90 may mediate these effects. These results indicate that EF-24 is a viable option for the prevention and treatment of PTC. [ABSTRACT FROM AUTHOR]

Cancer is the second leading cause of mortality worldwide. Conventional therapies, including surgery, radiation, and chemotherapy, have limited success because of secondary resistance. Therefore, safe, non-resistant, less toxic, and convenient drugs are urgently required. Natural products (NPs), primarily sourced from medicinal plants, are ideal for cancer treatment because of their low toxicity and high success. NPs cure cancer by regulating different pathways, such as PI3K/AKT/mTOR, ER stress, JNK, Wnt, STAT3, MAPKs, NF-kB, MEK-ERK, inflammation, oxidative stress, apoptosis, autophagy, mitophagy, and necroptosis. Among the NPs, steroid saponins, including polyphyllins (I, II, D, VI, and VII), have potent pharmacological, analgesic, and anticancer activities for the induction of cytotoxicity. Recent research has demonstrated that polyphyllins (PPs) possess potent effects against different cancers through apoptosis, autophagy, inflammation, and necroptosis. This review summarizes the available studies on PPs against cancer to provide a basis for future research. [ABSTRACT FROM AUTHOR]

Increasing evidence has shown that long non-coding RNAs (lncRNAs) have important biological functions and can be used as a prognostic biomarker in human cancers. However, investigation of the prognostic value of lncRNAs in head and neck squamous cell carcinoma (HNSCC) is in infancy. In the present study, we analyzed the lncRNA expression data in a large number of HNSCC patients (n=425) derived from The Cancer Genome Atlas (TCGA) to identify an lncRNA expression signature for improving the prognosis of HNSCC. Three lncRNAs are identified to be significantly associated with survival in the training dataset using Cox regression analysis. Three lncRNAs were integrated to construct an lncRNA expression signature that could stratify patients of training dataset into the high-risk group and low-risk group with significantly different survival time (median survival 1.85 years vs. 5.48 years; P=0.0018, log-rank test). The prognostic value of this three-lncRNA signature was confirmed in the testing and entire datasets, respectively. Further analysis revealed that the prognostic power of three-lncRNA signature was independent of clinical features by multivariate Cox regression and stratified analysis. These three lncRNAs were significantly associated with known genetic and epigenetic events by means of functional enrichment analysis. Therefore, our results indicated that the three-lncRNA expression signature can predict HNSCC patients' survival. [ABSTRACT FROM AUTHOR]

Ulinastatin exhibits anti-inflammatory activity and protects the heart from ischemia/reperfusion injury. However, whether ulinastatin has a protective effect in diabetic cardiomyopathy is yet to be elucidated. The aim of the present study was to investigate the protective effects of ulinastatin against diabetic cardiomyopathy and its underlying mechanisms. A C57/BL6J mice model of diabetic cardiomyopathy was used and mice were randomly assigned to three groups: Control group, diabetes mellitus (DM) group and DM + ulinastatin treatment group. Cardiac function was assessed using echocardiography and the level of inflammatory cytokine high mobility group box 1 (HMGB1) expression was measured using histopathological examination and reverse transcription-quantitative polymerase chain reaction. The levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 were measured using western blotting and ELISA. The apoptosis rate in the myocardium was assessed by TUNEL assay. Caspase-3 activation, expression of B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated x (Bax) were measured using western blotting, as was the activity of the mitogen activated protein kinase (MAPK) signaling pathway. The results indicated that ulinastatin significantly improved cardiac function in mice with DM. Ulinastatin treatment significantly downregulated HMGB1, TNF-α and IL-6 expression (P<0.05) and significantly reduced the percentage of apoptotic cardiomyocytes (P<0.05) via reduction of caspase-3 activation and the ratio of Bax/Bcl-2 in diabetic hearts (P<0.05). In addition, ulinastatin attenuated the activation of the MAPK signaling pathway. In conclusion, ulinastatin had a protective effect against DM-induced cardiac dysfunction in a mouse model. This protective effect may be associated with the anti-inflammatory and anti-apoptotic abilities of ulinastatin via the MAPK signaling pathway. [ABSTRACT FROM AUTHOR]