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1.
Heliyon ; 10(1): e23568, 2024 Jan 15.
Article in English | MEDLINE | ID: mdl-38187338

ABSTRACT

Group photos have become indispensable in various gathering scenarios, such as family reunions, friends' gatherings, competitions, conferences, store openings, and school graduation ceremonies. The researchers tried automatically adding people who could not participate in the group photo. However, the current research on generating the pose or position of the person by context prediction of the group photo ignores the individual attributes (such as height and body shape) of the target person and does not consider the pose and boundary of the person at the same time. To address these issues, we propose a virtual group photography model that combines the global context of a group photo and the individual attributes of the target person. The model is divided into two stages. The first stage is to predict the person's position, pose, and boundary in the new group photo based on the context of the input group photo and the person's characteristics. The second stage generates new group photos based on the first stage's pose and boundary results. The experimental results show that our method can significantly improve the harmony and authenticity of the synthesis of people in group photos and synthesize the characters that should exist in the group photo, which is very suitable for the field of group photos.

2.
Oncol Res ; 26(4): 565-572, 2018 May 07.
Article in English | MEDLINE | ID: mdl-28893348

ABSTRACT

Glypican 5 (GPC5) belongs to the family of heparan sulfate proteoglycans (HSPGs). It was initially known as a regulator of growth factors and morphogens. Recently, there have been reports on its correlation with the tumorigenic process in the development of some cancers. However, little is known about its precise role in prostate cancer (PCa). In the present study, we explored the expression pattern and biological functions of GPC5 in PCa cells. Our results showed that GPC5 was lowly expressed in PCa cell lines. Upregulation of GPC5 significantly inhibited PCa cell proliferation and invasion in vitro as well as attenuated tumor growth in vivo. We also found that overexpression of GPC5 inhibited the epithelial-mesenchymal transition (EMT) and Wnt/ß-catenin signaling activation, which was mediated by Sp1. Taken together, we suggest GPC5 as a tumor suppressor in PCa and provide promising therapeutic strategies for PCa.


Subject(s)
Cell Proliferation/genetics , Epithelial-Mesenchymal Transition/genetics , Glypicans/genetics , Prostatic Neoplasms/genetics , Sp1 Transcription Factor/metabolism , Wnt Signaling Pathway/genetics , Animals , Cell Line, Tumor , Humans , Male , Mice, Inbred BALB C , Neoplasm Invasiveness , Prostatic Neoplasms/metabolism , Up-Regulation , Xenograft Model Antitumor Assays
3.
J Cancer Res Clin Oncol ; 143(11): 2189-2200, 2017 Nov.
Article in English | MEDLINE | ID: mdl-28730284

ABSTRACT

PURPOSE: Osteosarcoma (OS) is one of the most prevalent primary malignant bone tumors in adolescent. HOTAIR is highly expressed and associated with the epigenetic modifications, especially DNA methylation, in cancer. However, the regulation mechanism between HOTAIR and DNA methylation and the biological effects of them in the pathogenesis of osteosarcoma remains elusive. METHOD: Through RNA-sequencing and computational analysis, followed by a variety of experimental validations, we report a novel interplay between HOTAIR, miR-126, and DNA methylation in OS. RESULTS: We found that HOTAIR is highly expressed in OS cells and the knockdown of HOTAIR leads to the down-regulation of DNMT1, as well as the decrease of global DNA methylation level. RNA-sequencing analysis of HOTAIR-regulated gene shows that CDKN2A is significantly repressed by HOTAIR. A series of experiments show that HOTAIR represses the expression of CDKN2A through inhibiting the promoter activity of CDKN2A by DNA hypermethylation. Further evidence shows that HOTAIR activates the expression of DNMT1 through repressing miR-126, which is the negative regulator of DNMT1. Functionally, HOTAIR depletion increases the sensibility of OS cells to DNMT1 inhibitor through regulating the viability and apoptosis of OS cells via HOTAIR-miR126-DNMT1-CDKN2A axis. CONCLUSION: These results not only enrich our understanding of the regulation relationship between non-coding RNA, DNA methylation, and gene expression, however, also provide a novel direction in developing more sophisticated therapeutic strategies for OS patients.


Subject(s)
Bone Neoplasms/genetics , DNA Methylation , Epigenesis, Genetic/genetics , Gene Expression Regulation, Neoplastic , Osteosarcoma/genetics , RNA, Long Noncoding/genetics , Apoptosis , Bone Neoplasms/pathology , Bone Neoplasms/therapy , Cell Proliferation , Cyclin-Dependent Kinase Inhibitor p16/genetics , DNA (Cytosine-5-)-Methyltransferase 1 , DNA (Cytosine-5-)-Methyltransferases/genetics , Humans , MicroRNAs/genetics , Osteosarcoma/pathology , Osteosarcoma/therapy , Promoter Regions, Genetic , Tumor Cells, Cultured
4.
Inflamm Res ; 65(1): 33-41, 2016 Jan.
Article in English | MEDLINE | ID: mdl-26525359

ABSTRACT

OBJECTIVE AND DESIGN: Isorhamnetin (Isor), a 3-O-methylated metabolite of quercetin, has shown antioxidant and anti-proliferative effects in previous studies. In this study, we investigated the anti-inflammatory effect of Isor on LPS-induced acute lung injury (ALI). Accordingly, we evaluated the effect of Isor on cytokine production elevated by LPS (1 µg/ml) in vitro. An in vivo ALI murine model was also established via lipopolysaccharide inhalation (LPS, 20 mg/kg), and the cytokine levels and inflammatory cell count in bronchoalveolar lavage fluid (BALF) were evaluated. The observed lung injury was assessed using histopathologic sections via H&E straining. Furthermore, to investigate whether the anti-inflammatory effect of Isor is associated with NF-κB and MAPKs pathway activation, the phosphorylated levels of ERK, JNK, IκBa and NF-κB(p65) were determined. RESULTS: Isor significantly inhibited LPS-induced TNF-α, IL-1ß and IL-6 secretion both in vitro and in vivo. Neutrophil infiltration and edema in an ALI model were substantially alleviated. The histopathological changes induced by LPS were lessened by Isor. Additionally, Isor notably suppressed the phosphorylation of ERK, JNK, IκBa and NF-κB(p65) activated by LPS in vivo. CONCLUSIONS: Isor showed efficient protective effects on an LPS-induced ALI model. MAPKs and NF-κB pathways are critical for Isor to perform its protective effects.


Subject(s)
Acute Lung Injury/chemically induced , Acute Lung Injury/prevention & control , Anti-Inflammatory Agents/therapeutic use , Lipopolysaccharides/antagonists & inhibitors , Lipopolysaccharides/toxicity , Quercetin/analogs & derivatives , Acute Lung Injury/pathology , Animals , Bronchoalveolar Lavage Fluid/cytology , Cytokines/biosynthesis , Lung/pathology , MAP Kinase Signaling System/drug effects , Male , Mice , Mice, Inbred BALB C , Mitogen-Activated Protein Kinases/metabolism , NF-kappa B/metabolism , Neutrophil Infiltration/drug effects , Pulmonary Edema/chemically induced , Pulmonary Edema/pathology , Quercetin/therapeutic use , RAW 264.7 Cells
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