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Search Results: 1 - 10 of 62094 matches for " Tze-Yi Lin "
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MicroRNA-22E Inhibits HER-3 Protein Expression to Facilitate Metastasis of Lung Adenocarcinomas  [PDF]
Hsin-Yuan Fang, Tze-Yi Lin, Shiow-Her Chiou, Liang-Shun Wang, Kuan-Chih Chow
Journal of Cancer Therapy (JCT) , 2015, DOI: 10.4236/jct.2015.64039
Abstract:

MicroRNA-22 (miR-22), a short non-coding RNA that post-transcriptionally regulates mRNA stability and protein synthesis, has been shown to enhance metastatic potential and to suppress HER-3, an important mRNA marker for non-small cell lung cancer (NSCLC). However, the effect of miR-22 has not been investigated in lung adenocarcinoma (LADC), the most common type of NSCLC in the Far East. In this study, we analyzed the role of miR-22 expression in LADC patients. Expression of miR-22 was detected by reverse-transcription polymerase chain reaction (RT-PCR), and confirmed by cDNA sequencing. Signals of miR-22 in LADC sections were identified using in situ hybridization (ISH). The association between miR-22 expression and survival was evaluated by the log-rank test. Induction of miR-22 expression and the effect on HER-3 levels, as well as the subsequent cell behavior were also investigated In vitro. Two types of miR-22: miR-22 and miR-22H, were detected by RT-PCR. The miR-22H had extra 13 bases, 5’-TGTGTTCAGTGGT-3’, at the 3’-end, and this segment was named miR-22E. Using ISH, miR-22E overexpression was detected in 225 (83.0%) of 271 LADC patients. A significant difference was found in cumulative survival between patients with high miR-22E levels and those with low miR-22E levels (p < 0.0001). In vitro, epidermal growth factor induced miR-22, but reduced HER-3 expression. Expression of miR-22 increased cell movement ability. In conclusion, expression of miR-22 is closely associated with tumor recurrence, metastasis and overall survival in LADC patients by suppressing HER-3 protein expression to enhance epithelial-mesenchymal transition and metastasis.

CD8+ Treg Cells Associated with Decreasing Disease Activity after Intravenous Methylprednisolone Pulse Therapy in Lupus Nephritis with Heavy Proteinuria
Yi-Giien Tsai, Chia-Ying Lee, Tze-Yi Lin, Ching-Yuang Lin
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0081344
Abstract: We focus on the role of CD8+ Treg cell in Intravenous methyl-prednisolone (IVMP) pulse therapy in forty patients with active Class III/IV childhood lupus nephritis (LN) with heavy proteinuria. IVMP therapy for five days. From peripheral blood mononuclear cells (PBMCs) and renal tissues, we saw IVMP therapy definitely restoring both CD4+CD25+FoxP3+ and CD8+CD25+Foxp3+ Treg cell number plus greater expression with intracellular IL-10 and granzyme B in CD8+FoxP3+ Treg from PBMCs. IVMP-treated CD8+CD25+ Treg cells directly suppressed CD4+ T proliferation and induced CD4+CD45RO+ apoptosis. Histologically, CD4+FoxP3+ as well as CD8+FoxP3+ Treg cells appeared in renal tissue of LN patients before IVMP by double immunohistochemical stain. CD8+FoxP3+ Treg cells increased in 10 follow-up renal biopsy specimens after IVMP. Reverse correlation of serum anti-C1q antibody and FoxP3+ Treg cells in PBMNCs (r = ?0.714, P<0.01). After IVMP, serum anti-C1q antibody decrease accompanied increase of CD4+FoxP3+ Treg cells. CD8+Treg cells reduced interferon-r response in PBMCs to major peptide autoepitopes from nucleosomes after IVMP therapy; siRNA of FoxP3 suppressed granzyme B expression while decreasing CD8+CD25+Treg-induced CD4+CD45RO+ apoptosis. Renal activity of LN by SLEDAI-2k in childhood LN was significantly higher than two weeks after IVMP (P<0.01). CD8+FoxP3+ Treg cells return in post-IVMP therapy and exert crucial immune modulatory effect to control autoimmune response in LN. Trial Registration DMR97-IRB-259
Hyperglycemia: GDNF-EGR1 Pathway Target Renal Epithelial Cell Migration and Apoptosis in Diabetic Renal Embryopathy
Ching-Yuang Lin, Tze-Yi Lin, Min-Chun Lee, Shih-Chieh Chen, Jeng-Shou Chang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056731
Abstract: Maternal hyperglycemia can inhibit morphogenesis of ureteric bud branching, Glial cell line-derived neurotrophilic factor (GDNF) is a key regulator of the initiation of ureteric branching. Early growth response gene-1 (EGR-1) is an immediate early gene. Preliminary study found EGR-1 persistently expressed with GDNF in hyperglycemic environment. To evaluate the potential relationship of hyperglycemia-GDNF-EGR-1 pathway, in vitro human renal proximal tubular epithelial (HRPTE) cells as target and in vivo streptozotocin-induced mice model were used. Our in vivo microarray, real time-PCR and confocal morphological observation confirmed apoptosis in hyperglycemia-induced fetal nephropathy via activation of the GDNF/MAPK/EGR-1 pathway at E12-E15. Detachment between ureteric branch and metanephrons, coupled with decreasing number and collapse of nephrons on Day 1 newborn mice indicate hyperglycemic environment suppress ureteric bud to invade metanephric rudiment. In vitro evidence proved that high glucose suppressed HRPTE cell migration and enhanced GDNF-EGR-1 pathway, inducing HRPTE cell apoptosis. Knockdown of EGR-1 by siRNA negated hyperglycemic suppressed GDNF-induced HRPTE cells. EGR-1 siRNA also reduced GDNF/EGR-1-induced cRaf/MEK/ERK phosphorylation by 80%. Our findings reveal a novel mechanism of GDNF/MAPK/EGR-1 activation playing a critical role in HRPTE cell migration, apoptosis and fetal hyperglycemic nephropathy.
HIV-1 Vpr Triggers Mitochondrial Destruction by Impairing Mfn2-Mediated ER-Mitochondria Interaction
Chih-Yang Huang, Shu-Fen Chiang, Tze-Yi Lin, Shiow-Her Chiou, Kuan-Chih Chow
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0033657
Abstract: Human immunodeficiency virus 1 (HIV-1) viral protein R (Vpr) has been shown to induce host cell death by increasing the permeability of mitochondrial outer membrane (MOM). The mechanism underlying the damage to the mitochondria by Vpr, however, is not clearly illustrated. In this study, Vpr that is introduced, via transient transfection or lentivirus infection, into the human embryonic kidney cell line HEK293, human CD4+ T lymphoblast cell line SupT1, or human primary CD4+ T cells serves as the model system to study the molecular mechanism of Vpr-mediated HIV-1 pathogenesis. The results show that Vpr injures MOM and causes a loss in membrane potential (MMP) by posttranscriptionally reducing the expression of mitofusin 2 (Mfn2) via VprBP-DDB1-CUL4A ubiquitin ligase complex, gradually weakening MOM, and increasing mitochondrial deformation. Vpr also markedly decreases cytoplasmic levels of dynamin-related protein 1 (DRP1) and increases bulging in mitochondria-associated membranes (MAM), the specific regions of endoplasmic reticulum (ER) which form physical contacts with the mitochondria. Overexpression of Mfn2 and DRP1 significantly decreased the loss of MMP and apoptotic cell death caused by Vpr. Furthermore, by employing time-lapse confocal fluorescence microscopy, we identify the transport of Vpr protein from the ER, via MAM to the mitochondria. Taken together, our results suggest that Vpr-mediated cellular damage may occur on an alternative protein transport pathway from the ER, via MAM to the mitochondria, which are modulated by Mfn2 and DRP1.
AKT/mTOR as Novel Targets of Polyphenol Piceatannol Possibly Contributing to Inhibition of Proliferation of Cultured Prostate Cancer Cells
Tze-Chen Hsieh,Chia-Yi Lin,Hung-Yun Lin,Joseph M. Wu
ISRN Urology , 2012, DOI: 10.5402/2012/272697
Abstract:
Biochemical and Cellular Evidence Demonstrating AKT-1 as a Binding Partner for Resveratrol Targeting Protein NQO2
Tze-chen Hsieh, Chia-Yi Lin, Dylan John Bennett, Erxi Wu, Joseph M. Wu
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0101070
Abstract: Background AKT plays an important role in the control of cell proliferation and survival. Aberrant activation of AKT frequently occurs in human cancers making it an attractive drug targets and leading to the synthesis of numerous AKT inhibitors as therapeutic candidates. Less is known regarding proteins that control AKT. We recently reported that quinone reductase 2 (NQO2) inhibited AKT activity, by unknown mechanisms. Methodology/Principal Findings In this study, molecular modeling was used to query interaction between NQO2 and AKT. We found that pleckstrin homology (PH) and kinase domains of AKT bind to chains A and B of NQO2. Pull-down and deletion assays revealed that PH domain of AKT is essential for interaction with NQO2. Modeling analysis further revealed that kinase domain of AKT binds NQO2 in the vicinity of asparagine 161 located in the resveratrol-binding domain of NQO2. In studies to test whether exposure to resveratrol potentiates or diminishes AKT binding to NQO2, we showed that pre-binding by resveratrol in wild type but not histidine-161 (N161H) mutant NQO2 significantly affected this interaction. To obtain information on interplay between resveratrol and AKT, resveratrol affinity chromatography was performed. AKT binds with high affinity to the column suggesting that it is a target of resveratrol. The half-life of AKT mRNA decreased from ~4 h in control cells to ~1 h in NQO2-knockdown cells. The inhibition of AKT by resveratrol was attenuated in NQO2-expressing relative to NQO2-knockdown cells. Conclusion/Significance Both NQO2 and AKT are targets of resveratrol; NQO2:AKT interaction is a novel physiological regulator of AKT activation/function.
The Melanogenesis Alteration Effects of Achillea millefolium L. Essential Oil and Linalyl Acetate: Involvement of Oxidative Stress and the JNK and ERK Signaling Pathways in Melanoma Cells
Hsin-Yi Peng, Chih-Chien Lin, Hsun-Yen Wang, Ying Shih, Su-Tze Chou
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095186
Abstract: The mitogen-activated protein kinase (MAPK) family, including extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase (JNK)1/2 and p38 MAPK, is known to be activated by ultraviolet (UV) radiation in melanocytes to regulate melanin production. Reactive oxygen species (ROS) play important roles in the pathway of ERK and JNK activation. It has been established that the essential oil of Achillea millefolium L. (AM-EO) has activities that suppress the oxidative stress and inflammatory responses. Thus, we analyzed the effects of AM-EO on melanogenesis in melanocyte stimulating hormone (α-MSH) treated melanoma cells. The results demonstrated that AM-EO suppresses melanin production by decreasing tyrosinase activity through the regulation of the JNK and ERK signaling pathways. This effect might be associated with the AM-EO activity leading to the suppression of ROS, and linalyl acetate is its major functional component. Therefore, we propose that AM-EO has the potential to treat hyperpigmentation in the future.
Achillea millefolium L. Essential Oil Inhibits LPS-Induced Oxidative Stress and Nitric Oxide Production in RAW 264.7 Macrophages
Su-Tze Chou,Hsin-Yi Peng,Jaw-Cherng Hsu,Chih-Chien Lin,Ying Shih
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms140712978
Abstract: Achillea millefolium L. is a member of the Asteraceae family and has been used in folk medicine in many countries. In this study, 19 compounds in A. millefolium essential oil (AM-EO) have been identified; the major components are artemisia ketone (14.92%), camphor (11.64%), linalyl acetate (11.51%) and 1,8-cineole (10.15%). AM-EO can suppress the inflammatory responses of lipopolysaccharides (LPS)-stimulated RAW 264.7 macrophages, including decreased levels of cellular nitric oxide (NO) and superoxide anion production, lipid peroxidation and glutathione (GSH) concentration. This antioxidant activity is not a result of increased superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, but rather occurs as a result of the down-regulation of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and heme oxygenase-1 (HO-1) expression, thus reducing the inflammatory response. Therefore, AM-EO can be utilized in many applications, including the treatment of inflammatory diseases in the future.
SinicView: A visualization environment for comparisons of multiple nucleotide sequence alignment tools
Arthur Shih, DT Lee, Laurent Lin, Chin-Lin Peng, Shiang-Heng Chen, Yu-Wei Wu, Chun-Yi Wong, Meng-Yuan Chou, Tze-Chang Shiao, Mu-Fen Hsieh
BMC Bioinformatics , 2006, DOI: 10.1186/1471-2105-7-103
Abstract: In this paper, we present a versatile alignment visualization system, called SinicView, (for Sequence-aligning INnovative and Interactive Comparison VIEWer), which allows the user to efficiently compare and evaluate assorted nucleotide alignment results obtained by different tools. SinicView calculates similarity of the alignment outputs under a fixed window using the sum-of-pairs method and provides scoring profiles of each set of aligned sequences. The user can visually compare alignment results either in graphic scoring profiles or in plain text format of the aligned nucleotides along with the annotations information. We illustrate the capabilities of our visualization system by comparing alignment results obtained by MLAGAN, MAVID, and MULTIZ, respectively.With SinicView, users can use their own data sequences to compare various alignment tools or scoring systems and select the most suitable one to perform alignment in the initial stage of sequence analysis.With exponentially increasing genomic sequences available in the public domain [1-5] comparative genomics demonstrates its power to help biologists identify novel conserved and functional regions in genomes [6-9]. Based on the comparison of cross-species genomic sequences, biologists can understand the evolutionary relationship of genomic regions among species, discover conserved regions between different genomes, such as yeast species genomes [10], metazoan genomes [11], vertebrate genomes [12], and mammalian genomes [13], discover regulatory motifs in the yeast [14] and human promoters [15] or identify potential conserved non-genic sequences (CNGs) [16].However, genomic sequences can be megabase long and thus the traditional sequence alignment tools based on dynamic programming would not work efficiently due to their time and space complexities. To better tackle this problem, several tools for genomic sequence alignment have been proposed, such as pairwise sequence aligners like MUMmer [17], GS-Aligner [18]
Survival rate in nasopharyngeal carcinoma improved by high caseload volume: a nationwide population-based study in Taiwan
Ching-Chih Lee, Tze-Ta Huang, Moon-Sing Lee, Yu-Chieh Su, Pesus Chou, Shih-Hsuan Hsiao, Wen-Yen Chiou, Hon-Yi Lin, Sou-Hsin Chien, Shih-Kai Hung
Radiation Oncology , 2011, DOI: 10.1186/1748-717x-6-92
Abstract: Between 1998 and 2000, a total of 1225 patients were identified from the Taiwan National Health Insurance Research Database. Survival analysis, the Cox proportional hazards model, and propensity score were used to assess the relationship between 10-year survival rates and physician caseloads.As the caseload of individual physicians increased, unadjusted 10-year survival rates increased (p < 0.001). Using a Cox proportional hazard model, patients with NPC treated by high-volume physicians (caseload ≥ 35) had better survival rates (p = 0.001) after adjusting for comorbidities, hospital, and treatment modality. When analyzed by propensity score, the adjusted 10-year survival rate differed significantly between patients treated by high-volume physicians and patients treated by low/medium-volume physicians (75% vs. 61%; p < 0.001).Our data confirm a positive volume-outcome relationship for NPC. After adjusting for differences in the case mix, our analysis found treatment of NPC by high-volume physicians improved 10-year survival rate.The fact that increased caseload is associated with better patient outcomes has been noted for three decades in many areas of health care, including acute myocardial infarction, many types of high-risk surgeries, and cancer treatment [1,2]. The "practice makes perfect" hypothesis may be valid for certain procedures such as open-heart and vascular surgery and "selective referral" may in part account for this phenomenon [3,4]. However, such a positive volume-outcome relationship is not well validated for other procedures. Only a few studies have examined the effect of physician caseload on treatment outcome for head and neck cancers [5,6].Taiwan has a high incidence of nasopharyngeal carcinoma (NPC): the annual incidence rate is 6.17 per 100,000 as compared with < 1 per 100,000 in Western countries [7]. Radiotherapy or concurrent chemoradiotherapy (CCRT) is the principal treatment because NPC is anatomically inaccessible and highly sensitive t
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