Autophagy plays a protective role against apoptosis induced by toxicarioside N via the Akt/mTOR pathway in human gastric cancer SGC-7901 cells

Huan-ge Zhao,Song-lin Zhou,Ying-ying Lin,Hua Wang,Hao Fu Dai,Feng-Ying Huang 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.10

Toxicarioside N (Tox N), a natural product extract from Antiaris toxicaria, has been reported to induce apoptosis in human gastric cancer cells. However, the mechanism and actual role of autophagy in Tox N-induced apoptosis of human gastric cancer cells remains poorly understood. In the current study, we demonstrated that Tox N could induce autophagy by inhibiting the Akt/mTOR signaling pathway in SGC-7901 cells. Moreover, we found that the inhibition of autophagy by 3-methyladenine, an autophagy inhibitor, enhanced Tox N-induced apoptotic cell death. However, the stimulation of autophagy by rapamycin, an autophagy activator, remarkably suppressed Tox N-induced apoptosis, suggesting that autophagy plays a protective role in Tox N-induced apoptosis. Thus, the results from this study suggested that Tox N combination with an autophagy inhibitor might be a promising strategy to enhance the anticancer activity of Tox N for the treatment of human gastric cancer.

Toxicarioside N induces apoptosis in human gastric cancer SGC- 7901 cell by activating the p38MAPK pathway

Huan-ge Zhao,Song-lin Zhou,Ying-ying Lin,Hao Fu Dai,Feng-Ying Huang 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.1

Natural plant compounds with potent proliferationinhibition and apoptosis induction properties havebeen screened as novel anticancer drugs. Toxicarioside N(Tox N) was isolated from the seeds of the tropical plantAntiaris toxicaria in Hainan province, China. To ourknowledge, the effects that Tox N has on the apoptosis ofSGC-7901 cells and its potential mechanism have neverbeen investigated. In this study, we detected the anticanceractivities of Tox N and explored the potential mechanismin the human gastrointestinal cancer cell line SGC-7901. Here, we found that Tox N inhibited SGC-7901 cell growthin a dose- and time-dependent manner and induced apoptosisin cells based on cell morphology and flow cytometryanalyses. Additionally, the SGC-7901 cell treated with ToxN up-regulated the expression level of cleaved caspase-3/9and PARP, increased the Bax/Bcl-2 ratio, and led to therelease of cytochrome c into the cytoplasm. In addition,Tox N treatment led to the phosphorylation of p38MAPK. SB203580, a p38MAPK inhibitor, partially attenuated ToxN induced apoptosis by preventing the activation of caspase-3/9 and PARP. Our results indicated for the first timethat Tox N can induce SGC-7901 cells apoptosis by activatingthe p38MAPK pathway.

USP18 promotes the growth in hemangiomas by regulating PI3K/AKT pathway

Ke Huan,Ma Xiang,Zeng Ying,Lu Jingjing,Fu Guili 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.4

Background USP (ubiquitin-specific peptidase) 18 functions as deubiquitinating enzyme and participates in various human malignancies. The underlying mechanism involved in USP18-mediated hemangiomas progression has not been reported yet. Objective Immunohistochemistry analysis, qRT-PCR, and western blot were applied to detect USP18 expression in hemangioma tissues and cells. Lentiviral-mediated short hairpin RNA transfection was performed to silence USP18, and pcDNA-mediated USP18 over-expression was also performed. Cell Counting Kit-8 (CCK-8), colony formation assay and flow cytometry were applied to investigate cell viability, proliferation, and apoptosis, respectively. In vivo xenograft model was performed to detect function of USP18 on tumor growth. Results USP18 was enhanced in hemangioma tissues and cells compared to vascular endothelial tissues and vascular endothelial cells, respectively. Forced USP18 promoted cell viability and proliferation of human hemangioma endothelial cell (HemEC) and hemangioendothelioma endothelial cell (EOMA). Cell apoptosis of HemEC and EOMA were repressed by USP18 over-expression with reduced Bax and cleaved caspase-3. In contrast, silence of USP18 demonstrated the opposite effects on HemEC and EOMA cell viability, proliferation, and apoptosis. Silence of USP18 also retarded in vivo tumorigenicity of hemangiomas. Phosphorylation of AKT was enhanced by USP18 over-expression, while reduced by USP18 silence. Conclusion USP18 functioned as an oncogene in hemangiomas through acceleration of cell proliferation and repression of cell apoptosis, providing new insight for therapy of hemangiomas. Background USP (ubiquitin-specific peptidase) 18 functions as deubiquitinating enzyme and participates in various human malignancies. The underlying mechanism involved in USP18-mediated hemangiomas progression has not been reported yet. Objective Immunohistochemistry analysis, qRT-PCR, and western blot were applied to detect USP18 expression in hemangioma tissues and cells. Lentiviral-mediated short hairpin RNA transfection was performed to silence USP18, and pcDNA-mediated USP18 over-expression was also performed. Cell Counting Kit-8 (CCK-8), colony formation assay and flow cytometry were applied to investigate cell viability, proliferation, and apoptosis, respectively. In vivo xenograft model was performed to detect function of USP18 on tumor growth. Results USP18 was enhanced in hemangioma tissues and cells compared to vascular endothelial tissues and vascular endothelial cells, respectively. Forced USP18 promoted cell viability and proliferation of human hemangioma endothelial cell (HemEC) and hemangioendothelioma endothelial cell (EOMA). Cell apoptosis of HemEC and EOMA were repressed by USP18 over-expression with reduced Bax and cleaved caspase-3. In contrast, silence of USP18 demonstrated the opposite effects on HemEC and EOMA cell viability, proliferation, and apoptosis. Silence of USP18 also retarded in vivo tumorigenicity of hemangiomas. Phosphorylation of AKT was enhanced by USP18 over-expression, while reduced by USP18 silence. Conclusion USP18 functioned as an oncogene in hemangiomas through acceleration of cell proliferation and repression of cell apoptosis, providing new insight for therapy of hemangiomas.

Human-Robot Interaction with Multi-Human Social Pattern Inference on a Multi-Modal Robot

Shih-Huan Tseng,Tung-Yen Wu,Ching-Ying Cheng,Li-Chen Fu 제어로봇시스템학회 2014 제어로봇시스템학회 국제학술대회 논문집 Vol.2014 No.10

To enable service robots enter a multi-human office environment, it is important to find a group of human users’ social patterns and then to provide a proper service to them in time. Usually, human users’ social patterns are represented in terms of nonverbal social signals. In this paper, some nonverbal social signals are fast detected in social environments. Then, robot can find the spatial social patterns of human users. Those patterns are indicated to human-to-human, human-to-robot or multi-human-to-robot interaction. Experimental results shows that our robot successfully find the aforementioned users’ social patterns.

A Novel Algorithm for Improving the SINR of D2D Communication in the Cellular Network

Cheng Huan,Youhua Fu,Jin Wang 보안공학연구지원센터 2016 International Journal of Future Generation Communi Vol.9 No.6

In this paper, we investigate the interference scenario where multiple Device-to-Device (D2D) pairs reuse the spectrum resources allocated to one cellular user, and propose a novel algorithm for improving the signal-to-interference-plus-noise ratio (SINR) of D2D communication. We call this D2D SINR improvement algorithm as DSIA, and design it from the perspective of precoding and decoding. With the DSIA, each D2D pair involved in the network can obtain the corresponding precoding and decoding vectors which make the SINR of its receiver being maximized. In order to clearly describe the design procedure of the proposed algorithm, we first formulate an optimization problem with multiple variables to maximize the SINR of each D2D receiver, then simplify the objective function through mathematical derivation and seek out the relationship between the optimized variables which can transform the optimization problem to one of solving nonlinear equations, and finally propose the DSIA to work out the nonlinear equations. Numerical results show that the DSIA will enable D2D to achieve significant performance gains in terms of SINR and bit-error rate (BER) compared with the traditional spectrum orthogonal scheme.

Upregulation and biological function of transmembrane protein 119 in osteosarcoma

Zhen-Huan Jiang,Jun Peng,Hui-Lin Yang,Xing-Li Fu,Jin-Zhi Wang,Lei Liu,Jian-Nong Jiang,Yong-Fei Tan,Zhi-Jun Ge 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

Osteosarcoma is suggested to be caused by genetic and molecular alterations that disrupt osteoblast differentiation. Recent studies have reported that transmembrane protein 119 (TMEM119) contributes to osteoblast differentiation and bone development. However, the level of TMEM119 expression and its roles in osteosarcoma have not yet been elucidated. In the present study, TMEM119 mRNA and protein expression was found to be up-regulated in osteosarcoma compared with normal bone cyst tissues. The level of TMEM119 protein expression was strongly associated with tumor size, clinical stage, distant metastasis and overall survival time. Moreover, gene set enrichment analysis (GSEA) of the Gene Expression Omnibus (GEO) GSE42352 dataset revealed TMEM119 expression in osteosarcoma tissues to be positively correlated with cell cycle, apoptosis, metastasis and TGF-β signaling. We then knocked down TMEM119 expression in U2OS and MG63 cells using small interfering RNA, which revealed that downregulation of TMEM119 could inhibit the proliferation of osteosarcoma cells by inducing cell cycle arrest in G0/G1 phase and apoptosis. We also found that TMEM119 knockdown significantly inhibited cell migration and invasion, and decreased the expression of TGF-β pathway-related factors (BMP2, BMP7 and TGF-β). TGF-β application rescued the inhibitory effects of TMEM119 knockdown on osteosarcoma cell migration and invasion. Further in vitro experiments with a TGF-β inhibitor (SB431542) or BMP inhibitor (dorsomorphin) suggested that TMEM119 significantly promotes cell migration and invasion, partly through TGF-β/BMP signaling. In conclusion, our data support the notion that TMEM119 contributes to the proliferation, migration and invasion of osteosarcoma cells, and functions as an oncogene in osteosarcoma.

Present Status and Future Trends on Urban Greening at Special Sites

Huinan Fu,hongye Huan Korean Institute of Landscape Architecture 2004 Journal of the Korean institute of landscape archi Vol.2 No.-

This paper discussed the use of the urban greening space beside nature land----special sites of urban Greening. Consider: the special sites of urban greening are referred to the space formed by urban building and framing, where plants can grow under natural or artificial condition. Filly using those spaces will efficiently increase green area, improving ecological environment and landscape in urban area. A classification to special sites of urban greening was put forward, which are the habits of plant combine with the form of buildings. The present status and future trends on urban greening at special sites was discussed and analyzed. Consider: there are two developing trends of the research of urban greening at special sites. Firstly, it is more naturalize and ecologize greening landscape. Secondly, It will take form a techologize in the process of constructing and materials.

SCHUR CONVEXITY OF L-CONJUGATE MEANS AND ITS APPLICATIONS

Chun-Ru Fu,Huan-Nan Shi,Dong-Sheng Wang Korean Mathematical Society 2023 대한수학회지 Vol.60 No.3

In this paper, using the theory of majorization, we discuss the Schur m power convexity for L-conjugate means of n variables and the Schur convexity for weighted L-conjugate means of n variables. As applications, we get several inequalities of general mean satisfying Schur convexity, and a few comparative inequalities about n variables Gini mean are established.

Molecular characterization, activity analysis and transcriptional detection of chitinases encoded in the genome of Spodoptera exigua

Lei Hea,Huan Yu,Cun-Yi Xu,Ying Zhao,Fu-Xiang Yang,Ya-Dong Guo,Guo-Hua Huang 한국응용곤충학회 2019 Journal of Asia-Pacific Entomology Vol.22 No.2

Insect chitinases are necessary hydrolytic enzymes for chitin degradation, insect molting and metamorphosis. In this study, five chitinases encoded in the genome of Spodoptera exigua (SeCHIT7, SeCHIT11, SeCHIT12, SeCHIT13 and SeCHIT14) were identified by reverse transcription PCR. Phylogenetic analysis indicated that SeCHIT7 belonged to Group III, and SeCHIT11/12/13/14 belonged to Group VIII. Real-time quantitative PCR analyses showed that SeCHIT7 had an extensive transcription at the fourth- and fifth-instar larval and pupal stages, while SeCHIT11 had the highest transcription level at the egg stage, and the transcription of SeCHIT12 increased by over 1000 times from pre-pupal to pupal stage. Tissue-specific analyses showed that these three SeCHITs (SeCHIT7, SeCHIT11 and SeCHIT12) were mainly transcribed in the midgut and fat body. Chitinase activity assays suggested that the activity had a lower level at the egg stage and peaked at the pupal stage. The activities were increased by 9.4 times from egg to first-instar larval stage. Tissue specificity analysis showed that the highest activity was observed in the fat body, followed by hemolymph and cuticle of the pre-pupal stage. Overall, these results provided valid information for further research on the biological function and regulation of chitinases in S. exigua.

Mutations of ARX and non-syndromic intellectual disability in Chinese population

Yufei Wu,Huan Zhang,Xiaofen Liu,Zhangyan Shi,Hongling Li,Zhibin Wang,Xiaoyong Jie,Shao-Ping Huang,Fu-Chang Zhang,Junlin Li,Ke-Jin Zhang,Xiao-Cai Gao 한국유전학회 2019 Genes & Genomics Vol.41 No.1

Mutations of Aristaless-related homeobox (ARX) gene were looked as the third cause of non-syndromic intellectual disability (NSID), while the boundary between true disease-causing mutations and non-disease-causing variants within this gene remains elusive. To investigate the relationship between ARX mutations and NSID, a panel comprising six reported causal mutations of the ARX was detected in 369 sporadic NSID patients and 550 random participants in Chinese. Two mutations, c.428_451 dup and p.G286S, may be disease-causing mutations for NSID, while p.Q163R and p.P353L showed a great predictive value in female NSID diagnosis with significant associations (X2 = 19.60, p = 9.54e−6 for p.Q163R; X2 = 25.70, p = 4.00e−07 for p.P353L), carriers of these mutations had an increased risk of NSID of more than fourfold. Detection of this panel also predicted significant associations between genetic variants of the ARX gene and NSID (p = 3.73e−4). The present study emphasized the higher genetic burden of the ARX gene on NSID in the Chinese population, molecular analysis of this gene should be considered for patients presenting NSID of unknown etiology.