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High dietary inorganic phosphate increases lung tumorigenesis and alters Akt signaling.
Jin, Hua,Xu, Cheng-Xiong,Lim, Hwang-Tae,Park, Sung-Jin,Shin, Ji-Young,Chung, Youn-Sun,Park, Se-Chang,Chang, Seung-Hee,Youn, Hee-Jeong,Lee, Kee-Ho,Lee, Yeon-Sook,Ha, Yoon-Cheol,Chae, Chan-Hee,Beck, Geo American Lung Association 2009 American journal of respiratory and critical care Vol.179 No.1
<P>RATIONALE: Phosphate (Pi) is an essential nutrient to living organisms. Recent surveys indicate that the intake of Pi has increased steadily. Our previous studies have indicated that elevated Pi activates the Akt signaling pathway. An increased knowledge of the response of lung cancer tissue to high dietary Pi may provide an important link between diet and lung tumorigenesis. OBJECTIVES: The current study was performed to elucidate the potential effects of high dietary Pi on lung cancer development. METHODS: Experiments were performed on 5-week-old male K-ras(LA1) lung cancer model mice and 6-week-old male urethane-induced lung cancer model mice. Mice were fed a diet containing 0.5% Pi (normal Pi) and 1.0% Pi (high Pi) for 4 weeks. At the end of the experiment, all mice were killed. Lung cancer development was evaluated by diverse methods. MEASUREMENT AND MAIN RESULTS: A diet high in Pi increased lung tumor progression and growth compared with normal diet. High dietary Pi increased the sodium-dependent inorganic phosphate transporter-2b protein levels in the lungs. High dietary consumption of Pi stimulated pulmonary Akt activity while suppressing the protein levels of tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 as well as Akt binding partner carboxyl-terminal modulator protein, resulting in facilitated cap-dependent protein translation. In addition, high dietary Pi significantly stimulated cell proliferation in the lungs of K-ras(LA1) mice. CONCLUSIONS: Our results showed that high dietary Pi promoted tumorigenesis and altered Akt signaling, thus suggesting that careful regulation of dietary Pi may be critical for lung cancer prevention as well as treatment.</P>
Inhibition of ID1–BMPR2 Intrinsic Signaling Sensitizes Glioma Stem Cells to Differentiation Therapy
Jin, Xiong,Jin, Xun,Kim, Leo J.Y.,Dixit, Deobrat,Jeon, Hee-Young,Kim, Eun-Jung,Kim, Jun-Kyum,Lee, Seon Yong,Yin, Jinlong,Rich, Jeremy N.,Kim, Hyunggee American Association for Cancer Research 2018 Clinical Cancer Research Vol.24 No.2
<P><B>Purpose:</B> Normal stem cells tightly control self-renewal and differentiation during development, but their neoplastic counterparts, cancer stem cells (CSCs), sustain tumorigenicity both through aberrant activation of stemness and evasion of differentiation. Although regulation of CSC stemness has been extensively studied, the molecular mechanisms suppressing differentiation remain unclear.</P><P><B>Experimental Design:</B> We performed <I>in silico</I> screening and <I>in vitro</I> validation studies through Western blotting, qRT-PCR for treatment of WNT and SHH signaling inhibitors, and BMP signaling inducer with control and ID1-overexpressing cells. We also performed <I>in vivo</I> drug treatment assays with Balb/c nude mice.</P><P><B>Results:</B> Inhibitor of differentiation 1 (ID1) abrogated differentiation signals from bone morphogenetic protein receptor (BMPR) signaling in glioblastoma stem cells (GSCs) to promote self-renewal. ID1 inhibited BMPR2 expression through miRNAs, miR-17 and miR-20a, which are transcriptional targets of MYC. ID1 increases MYC expression by activating WNT and SHH signaling. Combined pharmacologic blockade of WNT and SHH signaling with BMP treatment significantly suppressed GSC self-renewal and extended survival of tumor-bearing mice.</P><P><B>Conclusions:</B> Collectively, our results suggested that ID1 simultaneously regulates stemness through WNT and SHH signaling and differentiation through BMPR-mediated differentiation signaling in GSCs, informing a novel therapeutic strategy of combinatorial targeting of stemness and differentiation. <I>Clin Cancer Res; 24(2); 383–94. ©2017 AACR</I>.</P>
Jin, Hua,Kim, Hyun-Woo,Xu, Cheng-Xiong,Kwon, Jung-Taek,Hwang, Soon-Kyung,Lee, Eun-Sun,Chang, Seung-Hee,Park, Sung-Jin,Noh, Mi-Suk,Woo, Min-Ah,Yu, Kyeong-Nam,Lee, Hu-Jang,Choi, Joon-Weon,Choi, Don-Ha,C IOS Press 2007 Biofactors Vol.29 No.2
<P>Previously we reported that cadalene extracted from Zelkova serrata inhibited lung tumorigenesis in mice. However, the precise mechanism has not yet investigated. Here, we examined the effects of cadalene on signal pathways important for apoptosis, cell cycle, and protein translation in lung cancer cells. Our results showed that cadalene suppressed the expression of Akt and its phosphor-forms through controlling PI3K and PTEN. Cadalene also induced apoptosis through facilitating pro-apoptotic protein expression. In addition, cadalene caused cell cycle arrest and decreased mTOR-mediated protein translation. Taken together, cadalene may be developed as a lung cancer therapeutic agent in the future.</P>
A Composition Method of Logical Function Block Chain
JIN Rong,HE Xiong-xiong,Zhu Guang-xin 보안공학연구지원센터 2016 International Journal of Future Generation Communi Vol.9 No.3
ForCES is a new open programmable architecture, it separates control and forwarding, it also abstracts resources of Forwarding Elements (FE) into some Logical Function Blocks (LFB), Control Element (CE) can reconfigure the forwarding function of FEs by recomposing their LFB chains. Firstly, A SDN architecture based on ForCES is proposed. Then, based on the formalization of the concept of LFB and the traditional I/O matching algorithm, an LFB chain composition method is proposed. This method can combine a series of LFBs to an LFB chain according to special application request. Based on the LFB chain composition algorithm, an improved algorithm is proposed, which can improve the composition efficiency. At last, an example is provided to illustrate how this method works, and a simulation is given to compare the efficiency of the base algorithm and the improved algorithm.
Review of the Molecular Pathogenesis of Osteosarcoma
He, Jin-Peng,Hao, Yun,Wang, Xiao-Lin,Yang, Xiao-Jin,Shao, Jing-Fan,Guo, Feng-Jin,Feng, Jie-Xiong Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.15
Treating the osteosarcoma (OSA) remains a challenge. Current strategies focus on the primary tumor and have limited efficacy for metastatic OSA. A better understanding of the OSA pathogenesis may provide a rational basis for innovative treatment strategies especially for metastases. The aim of this review is to give an overview of the molecular mechanisms of OSA tumorigenesis, OSA cell proliferation, apoptosis, migration, and chemotherapy resistance, and how improved understanding might contribute to designing a better treatment target for OSA.
A Study on the Element of Total Tour Experience from UX Perspective
Zhou Xiong Jin,Young Hwan Pan 대한인간공학회 2016 대한인간공학회 학술대회논문집 Vol.2016 No.06
Objective: In order to design a new service for the traveler, all the cases that without any missing cases must to be considered. In this study, we starting from the traveler point of view and try to make the classification for the type of traveler’s activities that include all cases. Background: Unlike the past, we live in an age of information, and our travel behavior becomes more diverse. Diversification and spread of smart devices and more travel-related services made these images more obviously. According to this rapidly changing form of travel, to give travelers a better travel experience, some research is needed on travel behavior of the traveler’s point of view. Method: Through an analysis of the existing research, discovered the problems and improved the problems on the basis of the actual situation. Conclusion: Through this study, we are able to take a partial approach on design of travel. And allows the missing phenomenon does not occur. Application: The travel behavior models may help to discover new opportunities and insights on travel development.