Cynaropicrin inhibits lung cancer proliferation by targeting EGFR/AKT signaling pathway

Purpose: To investigate the anti-proliferative effect of cynaropicrin on lung cancer cell lines, and the underlying molecular mechanism. Methods: The effect of cynaropicrin treatment on the viabilities of H1975 and H460 cells was measured using Cell Counting Kit-8. Apoptosis was analysed by annexin-V/FITC staining, while protein expressions were assayed by western blotting. Results: Treatment of H1975 and H460 cells with cynaropicrin at doses of 0.25 – 2.0 μM led to a marked reduction in their viability (p < 0.05). In cynaropicrin-treated H1975 and H460 cells, there was significant increase in apoptosis, when compared to control cells. Caspase-3 and caspase-9 levels were also significantly increased in H1975 and H460 cells on treatment with cynaropicrin at doses of 0.25 and 2.0 μM while treatment with cynaropicrin at doses of 0.25 - 2.0 μM significantly down-regulated the mRNA expression of CCND1 in the two cell lines (p < 0.05). Cynaropicrin markedly inhibited mRNA and protein expressions of EGFR, and also downregulated AKT in H1975 and H460 cells (p < 0.05). However, cynaropicrin significantly increased the expressions of miR-202 and miR-370. Conclusion: Cynaropicrin exerts anti-proliferative and proapoptotic effects on H1975 and H460 lung cancer cells via deactivation of EGFR/AKT signaling pathway. Moreover, it upregulated the expressions of miR-202 and miR-370 in these cells. Thus, cynaropicrin has potentials for the treatment of lung cancer

MST4 Phosphorylation of ATG4B Regulates Autophagic Activity, Tumorigenicity, and Radioresistance in Glioblastoma

ATG4B stimulates autophagy by promoting autophagosome formation through reversible modification of ATG8. We identify ATG4B as a substrate of mammalian sterile20-like kinase (STK) 26/MST4. MST4 phosphorylates ATG4B at serine residue 383, which stimulates ATG4B activity and increases autophagic flux. Inhibition of MST4 or ATG4B activities using genetic approaches or an inhibitor of ATG4B suppresses autophagy and the tumorigenicity of glioblastoma (GBM) cells. Furthermore, radiation induces MST4 expression, ATG4B phosphorylation, and autophagy. Inhibiting ATG4B in combination with radiotherapy in treating mice with intracranial GBM xenograft markedly slows tumor growth and provides a significant survival benefit. Our work describes an MST4-ATG4B signaling axis that influences GBM autophagy and malignancy, and whose therapeutic targeting enhances the anti-tumor effects of radiotherapy., • MST4 kinase regulates the growth, sphere formation, and tumorigenicity of GBM cells • MST4 stimulates autophagy by activating ATG4B through phosphorylation of ATG4B S383 • Radiation increases MST4 expression and ATG4B phosphorylation, inducing autophagy • Inhibiting ATG4B enhances the anti-tumor effects of radiotherapy in GBM PDX models , Huang et al. show that radiation induces MST4 expression and that MST4 phosphorylates ATG4B at serine 383, which increases ATG4B activity and autophagic flux. Inhibition of ATG4B reduces autophagy and tumorigenicity of glioblastoma (GBM) cells and improves the impact of radiotherapy on GBM growth in mice

Adaptive Skin Color Detection Based on Human Face under Complex Background

Traditional skin color detection technique has a weak anti-interference ability against the pixels with color similar to skin under a complex background, and cannot reduce the influence of illumination on the characteristics of skin color. In this study, an adaptive skin color detection method is proposed to tackle the issues. The skin section containing illumination information is extracted by combining the face detection methods proposed by Haar and Adaboost, and using the improved binarization algorithm. Then, combining the best threshold of luminance component (Y) of skin color samples obtained after training in the YCbCr space, the improved histogram backprojection method is adopted to detect the skin color of the whole image. Experiments show that the method is robust under complex background and the influence of illumination. Moreover, the method has a higher accuracy and recall rate than traditional skin color detection methods

Adaptive Skin Color Detection Based on Human Face under Complex Background

Traditional skin color detection technique has a weak anti-interference ability against the pixels with color similar to skin under a complex background, and cannot reduce the influence of illumination on the characteristics of skin color. In this study, an adaptive skin color detection method is proposed to tackle the issues. The skin section containing illumination information is extracted by combining the face detection methods proposed by Haar and Adaboost, and using the improved binarization algorithm. Then, combining the best threshold of luminance component (Y) of skin color samples obtained after training in the YCbCr space, the improved histogram backprojection method is adopted to detect the skin color of the whole image. Experiments show that the method is robust under complex background and the influence of illumination. Moreover, the method has a higher accuracy and recall rate than traditional skin color detection methods

A DFT study of the electronic structures and optical properties of (Cr, C) co-doped rutile TiO2

To get an effective doping model of rutile TiO2, we systematically study geometrical parameters, density of states, electron densities, dielectric functions, optical absorption spectra for the pure, C mono-doping, Cr mono-doping and (Cr,C) co-doping rutile TiO2, using density functional calculations. We find that a C doped system presents higher stability under Ti-rich condition, while Cr doped and (Cr,C) co-doped systems are more stable under O-rich condition. For (Cr,C) co-doping situation, the imaginary part of the dielectric function reflects the higher energy absorption efficiency for incident photons. Moreover, co-doping system exhibits much bigger red-shift of optical absorption edge compared with Cr/C single doping systems, because of the great reduction of the direct band gap. The calculated optical absorption spectra show that the (Cr,C) co-doping rutile TiO2 has higher photocatalytic activity in the visible light region.Structural Mechanics Research La

Effects of extracorporeal circulation with different time on platelet count after cardiac surgery: a retrospective study based on medical records

Abstract Our objective was to observe the effects of extracorporeal circulation (ECC) with different time on platelet count in patients undergoing cardiac surgery. A total of 427 patients who underwent elective cardiac surgery under ECC in affiliated hospital of north Sichuan medical college from January 1, 2018 to July 31, 2021 were divided into three groups according to ECC time. We concluded that thrombocytopenia was common after ECC, maximum drop of the platelet counts after ECC was usually seen on the second day after ECC, and platelet counts started to recover on the fifth day after ECC. With the extension of ECC time, the drop in platelet counts is more pronounced, the volume of perioperative blood loss and blood products transfusion are more, and the recovery level and speed of platelet counts is lower

Androgen-Responsive Oncogenic lncRNA RP11-1023L17.1 Enhances c-Myc Protein Stability in Prostate Cancer

Long noncoding RNAs (lncRNAs) have been found as novel participants in the pathophysiology of prostate cancer (PCa), which is predominantly regulated by androgen and its receptor. The biological function of androgen-responsive lncRNAs remains poorly understood. Here, we identified that lncRNA RP11-1023L17.1, which is highly expressed in PCa. RP11-1023L17.1 expression, can be directly repressed by the androgen receptor in PCa cells. RP11-1023L17.1 depletion inhibited the proliferation, migration, and cell cycle progression, and promoted the apoptosis of PCa cells, indicating that RP11-1023L17.1 acts as an oncogene in PCa cells. Microarray results revealed that RP11-1023L17.1 depletion downregulated the c-Myc transcription signature in PCa cells. RP11-1023L17.1 depletion-induced cellular phenotypes can be overcome by ectopically overexpressed c-Myc. Mechanistically, RP11-1023L17.1 represses FBXO32 mRNA expression, thereby enhancing c-Myc protein stability by blocking FBXO32-mediated c-Myc degradation. Our findings reveal the previously unrecognized roles of RP11-1023L17.1 in c-Myc-dependent PCa tumorigenesis

An androgen reduced transcript of LncRNA GAS5 promoted prostate cancer proliferation

<div><p>Prostate cancer (PCa) becomes a leading cause of death in males nowadays. Recent reports showed that androgen-responsive long non-coding RNAs played important roles in tumorigenesis and progression of PCa. In this study, we focused on a special transcript of GAS5 (ENST00000456293.5, GAS5-007), which was reported as a tumor suppressor. Here, we demonstrated GAS5-007 was reduced by androgen treatment and inhibited by AR. Next, we explored the expression level of GAS, finding the expression of it in PCa tissue was higher than normal tissue in both public databases and human tissue samples. Functional analysis of GAS5 showed it was related to regulating translational elongation, protein biosynthesis, and transcription. Moreover, we observed GAS5-007 knockdown inhibited the proliferation, cell cycle and promoted cell apoptosis of PCa. We also constructed a GAS5-miRNA network to explain the different roles of different GAS5 transcripts in PCa. This study provides novel insights to identify potential diagnostic biomarker and therapy target for prostate cancer in clinical treatment.</p></div

Comprehensive Characterization of Androgen-Responsive lncRNAs Mediated Regulatory Network in Hormone-Related Cancers

The AR signaling pathway plays an important role in initiation and progression of many hormone-related cancers including prostate, bladder, kidney, lung, and breast cancer. However, the potential roles of androgen-responsive long noncoding RNAs (lncRNAs) in hormone-related cancers remained unclear. In the present study, we identified 469 novel androgen-responsive lncRNAs using microarray data. After validating the accuracy of the array data, we constructed a transcriptional network which contained more than 30 transcriptional factors using ChIP-seq data to explore upstream regulators of androgen-responsive lncRNAs. Next, we conducted bioinformatics analysis to identify lncRNA-miRNA-mRNA regulatory network. To explore the potential roles of androgen-responsive lncRNAs in hormone-related cancers, we performed coexpression network and PPI network analyses using TCGA data. GO and KEGG analyses showed these lncRNAs were mainly involved in regulating signal transduction, transcription, development, cell adhesion, immune response, cell differentiation, and MAPK signaling pathway. We also highlight the prognostic value of HPN-AS1, TPTEP1, and LINC00623 in cancer outcomes. Our results suggest that androgen-responsive lncRNAs played important roles in regulating hormone-related cancer progression and could be novel molecular biomarkers