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RISS 인기검색어
- 검색키워드
- 저자 : Dai Ying-Huan (검색결과 4 건)
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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.
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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.
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Inhibitory effects of piceatannol on human cytomegalovirus (hCMV) in vitro
Wang San-Ying,Zhang Jing,Xu Xiao-Gang,Su Hui-Li,Xing Wen-Min,Zhang Zhong-Shan,Jin Wei-Hua,Dai Ji-Huan,Wang Ya-Zhen,He Xin-Yue,Sun Chuan,Yan Jing,Mao Gen-Xiang 한국미생물학회 2020 The journal of microbiology Vol.58 No.8
Human cytomegalovirus (hCMV) is a ubiquitous herpesvirus, which results in the establishment of a latent infection that persists throughout the life of the host and can be reactivated when the immunity is low. Currently, there is no vaccine for hCMV infection, and the licensed antiviral drugs mainly target the viral enzymes and have obvious adverse reactions. Thus, it is important to search for compounds with antihCMV properties. The present study aimed to investigate the suppressive effects of piceatannol on hCMV Towne strain infection and the putative underlying mechanisms using human diploid fibroblast WI-38 cells. Piceatannol supplementation prevented the lytic changes induced by hCMV infection in WI-38 cells. Furthermore, piceatannol suppressed the expression of hCMV immediate-early (IE) and early (E) proteins as well as the replication of hCMV DNA in a dose-dependent manner. Moreover, hCMV-induced cellular senescence was suppressed by piceatannol, as shown by a decline in the senescence-associated β-galactosidase (SA-β-Gal) activity and decreased production of intracellular reactive oxygen species (ROS). p16INK4a, a major senescence-associated molecule, was dramatically elevated by current hCMV infection that was attenuated by pre-incubation with piceatannol in a dose-dependent manner. These results demonstrated that piceatannol suppressed the hCMV infection via inhibition of the activation of p16INK4a and cellular senescence induced by hCMV. Together, these findings indicate piceatannol as a novel and potent anti-hCMV agent with the potential to be developed as an effective treatment for chronic hCMV infection.
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Superenhancers as master gene regulators and novel therapeutic targets in brain tumors
Zhuang Hai-Hui,Qu Qiang,Teng Xin-Qi,Dai Ying-Huan,Qu Jian 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Transcriptional deregulation, a cancer cell hallmark, is driven by epigenetic abnormalities in the majority of brain tumors, including adult glioblastoma and pediatric brain tumors. Epigenetic abnormalities can activate epigenetic regulatory elements to regulate the expression of oncogenes. Superenhancers (SEs), identified as novel epigenetic regulatory elements, are clusters of enhancers with cell-type specificity that can drive the aberrant transcription of oncogenes and promote tumor initiation and progression. As gene regulators, SEs are involved in tumorigenesis in a variety of tumors, including brain tumors. SEs are susceptible to inhibition by their key components, such as bromodomain protein 4 and cyclin-dependent kinase 7, providing new opportunities for antitumor therapy. In this review, we summarized the characteristics and identification, unique organizational structures, and activation mechanisms of SEs in tumors, as well as the clinical applications related to SEs in tumor therapy and prognostication. Based on a review of the literature, we discussed the relationship between SEs and different brain tumors and potential therapeutic targets, focusing on glioblastoma.
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