Jing-Yi Lin
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Jing-Yi Lin has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
- Chun-I Pan
Department of Urology, New Taipei City Hospital, New Taipei City 112, Taiwan
1 shared publication - Chung-Sheng Shi
Graduate Institute of Clinical Medical Sciences, College of Medicine Chang Gung University Taoyuan Taiwan
1 shared publication - Fu-Shun Hsu
Department of Urology, New Taipei City Hospital, New Taipei City, Taiwan
1 shared publication - Hong-Chiang Chang
Department of Urology, National Taiwan University Hospital, Taipei, Taiwan
1 shared publication Hsin-Chun Ho
1 shared publication- Jo-Yu Hong
Department of Urology, National Taiwan University Hospital, Taipei 100, Taiwan
1 shared publication
Latest Publications
- Open Access
- 7 March 2019
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 20 (5) , 1162
Histone Deacetylase Inhibitor, Trichostatin A, Synergistically Enhances Paclitaxel-Induced Cytotoxicity in Urothelial Carcinoma Cells by Suppressing the ERK Pathway
Trichostatin A (TSA), an antifungal antibiotic derived from Streptomyces, inhibits mammalian histone deacetylases, and especially, selectively inhibits class I and II histone deacetylase (HDAC) families of enzymes. TSA reportedly elicits an antiproliferative response in multifarious tumors. This study investigated the antitumor effects of TSA alone and in combination with paclitaxel when applied to two high-grade urothelial carcinoma (UC) cell lines (BFTC-905 and BFTC-909). Fluorescence-activated cell sorting, flow cytometry, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium assay were used to assess TSA’s cytotoxicity and effects on apoptosis induction. TSA induced synergistic cytotoxicity, when combined with paclitaxel (combination index < 1), resulted in concomitant suppression of paclitaxel-induced activation of phospho-extracellular signal-regulated kinase (ERK) 1/2. A xenograft nude mouse model confirmed that TSA enhances the antitumor effects of paclitaxel. These findings demonstrate that the administration of TSA in combination with paclitaxel elicits a synergistic cytotoxic response. The results of this study indicate that the chemoresistance of UC could be circumvented by combining HDAC inhibitors to target the ERK pathway.
- 7 March 2019
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 20 (5) , 1162
Open AccessHistone Deacetylase Inhibitor, Trichostatin A, Synergistically Enhances Paclitaxel-Induced Cytotoxicity in Urothelial Carcinoma Cells by Suppressing the ERK Pathway
Trichostatin A (TSA), an antifungal antibiotic derived from Streptomyces, inhibits mammalian histone deacetylases, and especially, selectively inhibits class I and II histone deacetylase (HDAC) families of enzymes. TSA reportedly elicits an antiproliferative response in multifarious tumors. This study investigated the antitumor effects of TSA alone and in combination with paclitaxel when applied to two high-grade urothelial carcinoma (UC) cell lines (BFTC-905 and BFTC-909). Fluorescence-activated cell sorting, flow cytometry, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium assay were used to assess TSA’s cytotoxicity and effects on apoptosis induction. TSA induced synergistic cytotoxicity, when combined with paclitaxel (combination index < 1), resulted in concomitant suppression of paclitaxel-induced activation of phospho-extracellular signal-regulated kinase (ERK) 1/2. A xenograft nude mouse model confirmed that TSA enhances the antitumor effects of paclitaxel. These findings demonstrate that the administration of TSA in combination with paclitaxel elicits a synergistic cytotoxic response. The results of this study indicate that the chemoresistance of UC could be circumvented by combining HDAC inhibitors to target the ERK pathway.
- 12 March 2011
- Vol. 34 (1) , 44-9
Foot bacterial intertrigo mimicking interdigital tinea pedis.
Itchy maceration of the toe webs is common in warm and humid weather. Some cases do not respond to treatment for tinea or eczema. Patients with foot intertrigo with a poor response to antifungal or antiinflammatory treatment from 2004 to 2009 were included in this study. Their general characteristics were recorded. Bacterial and fungal cultures as well as potassium hydroxide preparations were performed. We recorded 32 episodes of foot bacterial intertrigo in 17 patients. The disease was more common in men (82%) and the mean age of the patients was 59 years. The main clinical finding was maceration of the toe webs. The majority of bacterial cultures grew mixed pathogens (93%). Pseudomonas aeruginosa, Enterococcus facealis and Staphylococcus aureus were the most common pathogens. Autoeczematization was present in 50% of the 32 disease episodes. Foot bacterial intertrigo is not a rare condition and can easily be confused with interdigital tinea or eczematous dermatitis. Proper identification of bacterial organisms is critical for early effective antibiotic therapy. Patients should be instructed about proper foot hygiene, which is important to prevent recurrent infections.
- 12 March 2011
- Vol. 34 (1) , 44-9
Foot bacterial intertrigo mimicking interdigital tinea pedis.
Itchy maceration of the toe webs is common in warm and humid weather. Some cases do not respond to treatment for tinea or eczema. Patients with foot intertrigo with a poor response to antifungal or antiinflammatory treatment from 2004 to 2009 were included in this study. Their general characteristics were recorded. Bacterial and fungal cultures as well as potassium hydroxide preparations were performed. We recorded 32 episodes of foot bacterial intertrigo in 17 patients. The disease was more common in men (82%) and the mean age of the patients was 59 years. The main clinical finding was maceration of the toe webs. The majority of bacterial cultures grew mixed pathogens (93%). Pseudomonas aeruginosa, Enterococcus facealis and Staphylococcus aureus were the most common pathogens. Autoeczematization was present in 50% of the 32 disease episodes. Foot bacterial intertrigo is not a rare condition and can easily be confused with interdigital tinea or eczematous dermatitis. Proper identification of bacterial organisms is critical for early effective antibiotic therapy. Patients should be instructed about proper foot hygiene, which is important to prevent recurrent infections.