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46 results on '"Hou, Ya-Chin"'

3. Dual targeted extracellular vesicles regulate oncogenic genes in advanced pancreatic cancer

Author

Chiang, Chi-Ling, Ma, Yifan, Hou, Ya-Chin, Pan, Junjie, Chen, Sin-Yu, Chien, Ming-Hsien, Zhang, Zhi-Xuan, Hsu, Wei-Hsiang, Wang, Xinyu, Zhang, Jingjing, Li, Hong, Sun, Lili, Fallen, Shannon, Lee, Inyoul, Chen, Xing-Yu, Chu, Yeh-Shiu, Zhang, Chi, Cheng, Tai-Shan, Jiang, Wen, Kim, Betty Y. S., Reategui, Eduardo, Lee, Robert, Yuan, Yuan, Liu, Hsiao-Chun, Wang, Kai, Hsiao, Michael, Huang, Chi-Ying F., Shan, Yan-Shen, Lee, Andrew S., and James Lee, L.

Published
2023
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8. Extracellular Vesicular Analysis of Glypican 1 mRNA and Protein for Pancreatic Cancer Diagnosis and Prognosis.

Author

Li, Hong, Chiang, Chi‐Ling, Kwak, Kwang Joo, Wang, Xinyu, Doddi, Sital, Ramanathan, Lakshmi V., Cho, Sun M., Hou, Ya‐Chin, Cheng, Tai‐Shan, Mo, Xiaokui, Chang, Yueh‐Shih, Chang, Hui‐Lan, Cheng, Weiming, Tsai, Wei‐Ni, Nguyen, Luong T. H., Pan, Junjie, Ma, Yifan, Rima, Xilal Y., Zhang, Jingjing, and Reategui, Eduardo

Subjects
CANCER diagnosis, CANCER prognosis, GENE expression, EXTRACELLULAR vesicles, PANCREATIC duct
Abstract

Detecting pancreatic duct adenocarcinoma (PDAC) in its early stages and predicting late‐stage patient prognosis undergoing chemotherapy is challenging. This work shows that the activation of specific oncogenes leads to elevated expression of mRNAs and their corresponding proteins in extracellular vesicles (EVs) circulating in blood. Utilizing an immune lipoplex nanoparticle (ILN) biochip assay, these findings demonstrate that glypican 1 (GPC1) mRNA expression in the exosomes‐rich (Exo) EV subpopulation and GPC1 membrane protein (mProtein) expression in the microvesicles‐rich (MV) EV subpopulation, particularly the tumor associated microvesicles (tMV), served as a viable biomarker for PDAC. A combined analysis effectively discriminated early‐stage PDAC patients from benign pancreatic diseases and healthy donors in sizable clinical from multiple hospitals. Furthermore, among late‐stage PDAC patients undergoing chemotherapy, lower GPC1 tMV‐mProtein and Exo‐mRNA expression before treatment correlated significantly with prolonged overall survival. These findings underscore the potential of vesicular GPC1 expression for early PDAC screenings and chemotherapy prognosis. [ABSTRACT FROM AUTHOR]

Published
2024
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21. Additional file 1 of Tumor-associated macrophages promote resistance of hepatocellular carcinoma cells against sorafenib by activating CXCR2 signaling

Author

Wang, Hao-Chen, Haung, Lin-Ya, Wang, Chih-Jung, Chao, Ying-Jui, Hou, Ya-Chin, Yen, Chia-Jui, and Shan, Yan-Shen

Abstract

Additional file 1: Figure S1. M2 polarization of U937 cell by coculture with HepG2 cells. U937 cells were cocultured with HepG2 cells for 72 h. U937 cells were then collected and subjected to flow cytometry with double staining for CD68 and CD204. Figure S2. Treatment with cytokines or coculture CM does not cause toxicity in U937 cells. A U937 cells were polarized towards TAMsCM and M2 MφsCyto by coculture CM and IL-4/IL-10, respectively, for 48 h. The nonadherent cells were collected for trypan blue assay and were visualized using bright field microscopy. Magnification: 100×. B U937 cells were incubated in normal RPMI medium or RPMI medium containing with 10% of coculture CM for 48 h. Total cells were collected for trypan blue assay, and an automated cell counter was used to count dead and live cells. The bar graphs depict the numbers of dead cells and live cells. NS, not significant vs. normal medium. Figure S3. Coculture with M2 TAMs further boosts sorafenib resistance of HepG2 sphere cells. HepG2 cells were cultured in ultra-low attachment surface dishes for 14 days to form spheres. The spheres were dispersed into single cells to monoculture and cocultured with TAMsCM or M2 MφsCyto for 72 h followed by SOR treatment at different concentrations for 48 h. Cell viability was determined by MTT assay. Figure S4. Pharmacological inhibition CXCR2 signaling reduces M2 TAMs-induced stemness. HepG2 cells were monocultured and cocultured with TAMsCM or M2 MφsCyto for 72 h. Conditioned media from monocultures and cocultures were collected to treat HepG2 cells in combination with SB225002 for 48 h followed by detecting mRNA expression of stemness genes including NANOG, SOX2, and OCT4 using qPCR. The bar graphs show relative mRNA expression of stemness genes. **, P

Published
2022
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26. The Fibronectin Expression Determines the Distinct Progressions of Malignant Gliomas via Transforming Growth Factor-Beta Pathway

Author

Chen, Chih-Wei, primary, Yang, Cheng-Han, additional, Lin, Yuan-Ho, additional, Hou, Ya-Chin, additional, Cheng, Tain-Junn, additional, Chang, Sheng-Tsung, additional, Huang, Yu-Hua, additional, Chung, Shang-Ting, additional, Chio, Chung-Ching, additional, Shan, Yan-Shen, additional, Cheng, Hung-Chi, additional, and Chang, Wen-Tsan, additional

Published
2021
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28. Low CD8+ T Cell Infiltration and High PD-L1 Expression Are Associated with CD44+/CD133+ Cancer Stem Cells and Predict an Unfavorable Prognosis in Pancreatic Cancer

Author

Hou, Ya-Chin, Chao, Ying-Jui, Hsieh, Min-Hua, Tung, Hui-Ling, Wang, Hao-Chen, and Shan, Yan-Shen

Subjects
oncology_oncogenics
Abstract

Cancer immunotherapy targeting immune checkpoints has exhibited promising clinical outcomes in many cancers, but it offers only limited benefits for pancreatic cancer (PC). Cancer stem cells (CSCs), a minor subpopulation of cancer cells, play important roles in tumor initiation, progression, and drug resistance. Accumulating evidence suggests that CSCs employ immunosuppressive effect to evade the immune recognition. However, clinical implications of the associations among CD8+ T cells infiltration, programmed death receptor ligand-1 (PD-L1) expression, and CSCs existence are poorly understood in PC. Immunostaining and quantitative analysis were performed to assess CD8+ T cells infiltration, PD-L1 expression, and their relationship with CD44+/CD133+ CSCs and disease progression in PC. CD8+ T cells infiltration was associated with better survival while PD-L1 expression was correlated with PC recurrence. Both the low CD8+ T cells infiltration/high PD-L1 expression group and the high CD8+ T cells infiltration/high PD-L1 expression group show high levels of CD44+/CD133+ CSCs, but patients with low CD8+ T cells infiltration/high PD-L1 expression had worse survival and higher recurrence risk than those with high CD8+ T cells infiltration/high PD-L1 expression. Moreover, CD8+ T cells infiltration could reduce unfavorable prognostic effect of high co-expression of PD-L1 and CD44/CD133. Our study highlights an interaction among CD8+ T cells infiltration, PD-L1 expression, and CD44+/CD133+ CSCs existence, which contributes to PC progression and immune evasion.

Published
2019

43. A Gene Expression Signature of Epithelial Tubulogenesis and a Role for ASPM in Pancreatic Tumor Progression

Author

Wang, Wei–Yu, primary, Hsu, Chung–Chi, additional, Wang, Ting–Yun, additional, Li, Chi–Rong, additional, Hou, Ya–Chin, additional, Chu, Jui–Mei, additional, Lee, Chung–Ta, additional, Liu, Ming–Sheng, additional, Su, Jimmy J.–M., additional, Jian, Kuan–Ying, additional, Huang, Shenq–Shyang, additional, Jiang, Shih–Sheng, additional, Shan, Yan–Shen, additional, Lin, Pin–Wen, additional, Shen, Yin–Ying, additional, Lee, Michael T.–L., additional, Chan, Tze–Sian, additional, Chang, Chun–Chao, additional, Chen, Chung–Hsing, additional, Chang, I–Shou, additional, Lee, Yen–Ling, additional, Chen, Li–Tzong, additional, and Tsai, Kelvin K., additional

Published
2013
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45. Blocking M2-Like Macrophage Polarization Using Decoy Oligodeoxynucleotide-Based Gene Therapy Prevents Immune Evasion for Pancreatic Cancer Treatment.

Author

Chen CJ, Wang HC, Hou YC, Wu YY, Shieh CC, and Shan YS

Subjects
Humans, Animals, Mice, Genetic Therapy methods, Cell Line, Tumor, NADPH Oxidase 2 genetics, NADPH Oxidase 2 metabolism, Reactive Oxygen Species metabolism, Tumor Escape drug effects, Xenograft Model Antitumor Assays, Disease Models, Animal, Gene Expression Regulation, Neoplastic drug effects, Macrophage Activation drug effects, U937 Cells, Pancreatic Neoplasms therapy, Pancreatic Neoplasms immunology, Pancreatic Neoplasms pathology, Pancreatic Neoplasms genetics, Pancreatic Neoplasms drug therapy, Oligodeoxyribonucleotides pharmacology, Macrophages metabolism, Macrophages immunology, Macrophages drug effects
Abstract

M2-like macrophages exhibit immunosuppressive activity and promote pancreatic cancer progression. Reactive oxygen species (ROS) affect macrophage polarization; however, the mechanism remains unclear. This study aimed to elucidate the underlying molecular basis and design a gene therapy to inhibit M2-like polarization. Microarray analysis and immunofluorescence staining were performed in M1-like and M2-like macrophages to ascertain the expression of CYBB, a major intracellular ROS source. Coculture assay and syngeneic orthotopic pancreatic cancer mice models were used to study the mechanism of M2-like skewing. Decoy oligodeoxynucleotides (ODNs) were designed to manipulate CYBB transcription to inhibit M2-like polarization and control tumor growth. Lipopolysaccharide treatment polarized U937 cells to M1-like macrophages in which CYBB expression was increased. In contrast, coculture with PANC-1 cells induced M2-like polarization in U937 cells with CYBB downregulation. High CD204 M2-like expression in combination with low CYBB expression was associated with the worst prognosis in patients with pancreatic cancer. STAT6 and HDAC2 in U937 cells were activated by cancer cell-derived IL4 after coculture and then bound to the CYBB promoter to repress CYBB expression, resulting in M2-like polarization. Diphenyleneiodonium, 8λ³-iodatricyclo[7.4.0.02,⁷]trideca-1(13),2,4,6,9,11-hexaen-8-ylium chloride that inhibits ROS production could block this action. Knockdown of STAT6 and HDAC2 also inhibited M2-like polarization and maintained the M1-like phenotype of U937 cells after coculture. Decoy ODNs interrupting the binding of STAT6 to the CYBB promoter counteracted M2-like polarization and tumor growth and triggered antitumor immunity in vivo. Gene therapy using STAT6-CYBB decoy ODNs can inhibit M2-like polarization, representing a potential therapeutic tool for pancreatic cancer., (©2024 The Authors; Published by the American Association for Cancer Research.)

Published
2024
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46. Pancreatic cancer cell-derived semaphorin 3A promotes neuron recruitment to accelerate tumor growth and dissemination.

Author

Hung YH, Hou YC, Hsu SH, Wang LY, Tsai YL, Shan YS, Su YY, Hung WC, and Chen LT

Abstract

Perineural invasion and neurogenesis are frequently observed in pancreatic ductal adenocarcinoma (PDAC), and they are associated with a poor prognosis. Axon guidance factor semaphorin 3A (SEMA3A) is upregulated in PDAC. However, it remains unclear whether cancer-derived SEMA3A influences nerve innervation and pancreatic tumorigenesis. In silico analyses were performed using PROGgene and NetworkAnalyst to clarify the importance of SEMA3A and its receptors, plexin A1 (PLXNA1) and neuropilin 2 (NRP2), in pancreatic cancer. In vitro assays, including migration, neurite outgrowth, and 3D recruitment, were performed to study the effects of SEMA3A on neuronal behaviors. Additionally, an orthotopic animal study using C57BL/6 mice was performed to validate the in vitro findings. Expression of SEMA3A and its receptors predicted worse prognosis for PDAC. Cancer-derived SEMA3A promoted neural migration, neurite outgrowth, and neural recruitment. Furthermore, SEMA3A-induced effects depended on PLXNA1, NRP2, and MAPK activation. Trametinib, an approved MAPK kinase (MEK) inhibitor, counteracted SEMA3A-enhanced neuronal activity in vitro . Inhibition of SEMA3A by shRNA in pancreatic cancer cells resulted in decreased neural recruitment, tumor growth, and dissemination in vivo . Our results suggested that cancer-secreted SEMA3A plays an important role in promoting neo-neurogenesis and progression of PDAC., Competing Interests: None., (AJCR Copyright © 2023.)

Published
2023

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