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28 results on '"Tang, Philip Chiu-Tsun"'

3. Hematopoietic Transcription Factor RUNX1 is Essential for Promoting Macrophage–Myofibroblast Transition in Non‐Small‐Cell Lung Carcinoma (Adv. Sci. 1/2024)

Author

Tang, Philip Chiu‐Tsun, primary, Chan, Max Kam‐Kwan, additional, Chung, Jeff Yat‐Fai, additional, Chan, Alex Siu‐Wing, additional, Zhang, Dongmei, additional, Li, Chunjie, additional, Leung, Kam‐Tong, additional, Ng, Calvin Sze‐Hang, additional, Wu, Yi, additional, To, Ka‐Fai, additional, Lan, Hui‐Yao, additional, and Tang, Patrick Ming‐Kuen, additional

Published
2024
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5. Hematopoietic Transcription Factor RUNX1 is Essential for Promoting Macrophage–Myofibroblast Transition in Non‐Small‐Cell Lung Carcinoma

Author

Tang, Philip Chiu‐Tsun, primary, Chan, Max Kam‐Kwan, additional, Chung, Jeff Yat‐Fai, additional, Chan, Alex Siu‐Wing, additional, Zhang, Dongmei, additional, Li, Chunjie, additional, Leung, Kam‐Tong, additional, Ng, Calvin Sze‐Hang, additional, Wu, Yi, additional, To, Ka‐Fai, additional, Lan, Hui‐Yao, additional, and Tang, Patrick Ming‐Kuen, additional

Published
2023
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6. TGF-β signaling networks in the tumor microenvironment

Author

Chan, Max Kam-Kwan, primary, Chung, Jeff Yat-Fai, additional, Tang, Philip Chiu-Tsun, additional, Chan, Alex Siu-Wing, additional, Ho, Johnny Yuk-Yeung, additional, Lin, Tony Pak-Tik, additional, Chen, Jiaoyi, additional, Leung, Kam-Tong, additional, To, Ka-Fai, additional, Lan, Hui-Yao, additional, and Tang, Patrick Ming-Kuen, additional

Published
2022
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7. Single-cell RNA sequencing uncovers a neuron-like macrophage subset associated with cancer pain

Author

Tang, Philip Chiu-Tsun, primary, Chung, Jeff Yat-Fai, additional, Liao, Jinyue, additional, Chan, Max Kam-Kwan, additional, Chan, Alex Siu-Wing, additional, Cheng, Guangyao, additional, Li, Chunjie, additional, Huang, Xiao-Ru, additional, Ng, Calvin Sze-Hang, additional, Lam, Eric W-F, additional, Zhang, Dongmei, additional, Ho, Yi-Ping, additional, To, Ka-Fai, additional, Leung, Kam-Tong, additional, Jiang, Xiaohua, additional, Ko, Ho, additional, Lee, Tin-Lap, additional, Lan, Hui-Yao, additional, and Tang, Patrick Ming-Kuen, additional

Published
2022
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8. LncRNA-Dependent Mechanisms of Transforming Growth Factor-β: From Tissue Fibrosis to Cancer Progression

Author

Tang, Philip Chiu-Tsun, primary, Zhang, Ying-Ying, additional, Li, Jane Siu-Fan, additional, Chan, Max Kam-Kwan, additional, Chen, Jiaoyi, additional, Tang, Ying, additional, Zhou, Yiming, additional, Zhang, Dongmei, additional, Leung, Kam-Tong, additional, To, Ka-Fai, additional, Tang, Sydney Chi-Wai, additional, Lan, Hui-Yao, additional, and Tang, Patrick Ming-Kuen, additional

Published
2022
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9. Smad3 Promotes Cancer‐Associated Fibroblasts Generation via Macrophage–Myofibroblast Transition (Adv. Sci. 1/2022)

Author

Tang, Philip Chiu‐Tsun, primary, Chung, Jeff Yat‐Fai, additional, Xue, Vivian Wei‐wen, additional, Xiao, Jun, additional, Meng, Xiao‐Ming, additional, Huang, Xiao‐Ru, additional, Zhou, Shuang, additional, Chan, Alex Siu‐Wing, additional, Tsang, Anna Chi‐Man, additional, Cheng, Alfred Sze‐Lok, additional, Lee, Tin‐Lap, additional, Leung, Kam‐Tong, additional, Lam, Eric W.‐F., additional, To, Ka‐Fai, additional, Tang, Patrick Ming‐Kuen, additional, and Lan, Hui‐Yao, additional

Published
2022
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10. USMB-shMincle: a virus-free gene therapy for blocking M1/M2 polarization of tumor-associated macrophages

Author

Xue, Vivian Weiwen, primary, Chung, Jeff Yat-Fai, additional, Tang, Philip Chiu-Tsun, additional, Chan, Alex Siu-Wing, additional, To, Travis Hoi-Wai, additional, Chung, Justin Shing-Yin, additional, Mussal, Francis, additional, Lam, Eric W.-F., additional, Li, Chunjie, additional, To, Ka-Fai, additional, Leung, Kam-Tong, additional, Lan, Hui-Yao, additional, and Tang, Patrick Ming-Kuen, additional

Published
2021
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11. Smad3 Promotes Cancer‐Associated Fibroblasts Generation via Macrophage–Myofibroblast Transition

Author

Tang, Philip Chiu‐Tsun, primary, Chung, Jeff Yat‐Fai, additional, Xue, Vivian Wei‐wen, additional, Xiao, Jun, additional, Meng, Xiao‐Ming, additional, Huang, Xiao‐Ru, additional, Zhou, Shuang, additional, Chan, Alex Siu‐Wing, additional, Tsang, Anna Chi‐Man, additional, Cheng, Alfred Sze‐Lok, additional, Lee, Tin‐Lap, additional, Leung, Kam‐Tong, additional, Lam, Eric W.‐F., additional, To, Ka‐Fai, additional, Tang, Patrick Ming‐Kuen, additional, and Lan, Hui‐Yao, additional

Published
2021
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12. AANG: A natural compound formula for overcoming multidrug resistance via synergistic rebalancing the TGF‐β/Smad signalling in hepatocellular carcinoma

Author

Chung, Jeff Yat‐Fai, primary, Chan, Max Kam‐Kwan, additional, Tang, Philip Chiu‐Tsun, additional, Chan, Alex Siu‐Wing, additional, Chung, Justin Shing‐Yin, additional, Meng, Xiao‐Ming, additional, To, Ka‐Fai, additional, Lan, Hui‐Yao, additional, Leung, Kam‐Tong, additional, and Tang, Patrick Ming‐Kuen, additional

Published
2021
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15. TGF-β1 Signaling: Immune Dynamics of Chronic Kidney Diseases

Author

Tang, Philip Chiu-Tsun, primary, Chan, Alex Siu-Wing, additional, Zhang, Cai-Bin, additional, García Córdoba, Cristina Alexandra, additional, Zhang, Ying-Ying, additional, To, Ka-Fai, additional, Leung, Kam-Tong, additional, Lan, Hui-Yao, additional, and Tang, Patrick Ming-Kuen, additional

Published
2021
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17. Transforming growth factor‐β signalling in renal fibrosis: from Smads to non‐coding RNAs

Author

Tang, Patrick Ming‐Kuen, Zhang, Ying‐Ying, Mak, Thomas Shiu‐Kwong, Tang, Philip Chiu‐Tsun, Huang, Xiao‐Ru, and Lan, Hui‐Yao

Subjects
RNA, Untranslated, Gene Expression Regulation, Transforming Growth Factor beta, Topical Reviews, Animals, Humans, Kidney Diseases, Smad Proteins, Fibrosis
Abstract

Transforming growth factor‐β (TGF‐β) is the key player in tissue fibrosis. However, antifibrotic therapy targeting this multifunctional protein may interfere with other physiological processes to cause side effects. Thus, precise therapeutic targets need to be identified by further understanding the underlying mechanisms of TGF‐β1 signalling during fibrogenesis. Equilibrium of Smad signalling is crucial for TGF‐β‐mediated renal fibrosis, where Smad3 is pathogenic but Smad2 and Smad7 are protective. The activation of TGF‐β1/Smad signalling triggers extracellular matrix deposition, and local myofibroblast generation and activation. Mechanistic studies have shown that TGF‐β/Smad3 transits the microRNA profile from antifibrotic to profibrotic and therefore promotes renal fibrosis via regulating non‐coding RNAs at transcriptional levels. More importantly, disease‐specific Smad3‐dependent long non‐coding RNAs have been recently uncovered from mouse kidney disease models and may represent novel precision therapeutic targets for chronic kidney disease. In this review, mechanisms of TGF‐β‐driven renal fibrosis via non‐coding RNAs and their translational capacities will be discussed in detail. [Image: see text]

Published
2018

18. A Novel Feeder-free System for Mass Production of Murine Natural Killer Cells In Vitro

Author

Tang, Patrick Ming-Kuen, Tang, Philip Chiu-Tsun, Chung, Jeff Yat-Fai, Hung, Jessica Shuk Chun, Wang, Qing-Ming, Lian, Guang-Yu, Sheng, Jingyi, Huang, Xiao-Ru, To, Ka-Fai, and Lan, Hui-Yao

Subjects
Killer Cells, Natural, Mice, Basic-Leucine Zipper Transcription Factors, Immunology, Cytological Techniques, Animals, Bone Marrow Cells, Cell Differentiation, Gene Silencing, RNA, Small Interfering, Cell Line
Abstract

Natural killer (NK) cells belong to the innate immune system and are a first-line anti-cancer immune defense; however, they are suppressed in the tumor microenvironment and the underlying mechanism is still largely unknown. The lack of a consistent and reliable source of NK cells limits the research progress of NK cell immunity. Here, we report an in vitro system that can provide high quality and quantity of bone marrow-derived murine NK cells under a feeder-free condition. More importantly, we also demonstrate that siRNA-mediated gene silencing successfully inhibits the E4bp4-dependent NK cell maturation by using this system. Thus, this novel in vitro NK cell differentiating system is a biomaterial solution for immunity research.

Published
2018

25. LRNA9884, a Novel Smad3-Dependent Long Noncoding RNA, Promotes Diabetic Kidney Injury in / Mice via Enhancing MCP-1-Dependent Renal Inflammation.

Author

Ying-ying Zhang, Patrick Ming-Kuen Tang, Philip Chiu-Tsun Tang, Jun Xiao, Xiao-Ru Huang, Chen Yu, Ma, Ronald C. W., Hui-Yao Lan, Zhang, Ying-Ying, Tang, Patrick Ming-Kuen, Tang, Philip Chiu-Tsun, Xiao, Jun, Huang, Xiao-Ru, Yu, Chen, and Lan, Hui-Yao

Subjects
NON-coding RNA, KIDNEY injuries, ADVANCED glycation end-products, CREATININE, MICE, DIABETIC nephropathies
Abstract

Transforming growth factor-β/Smad3 signaling plays an important role in diabetic nephropathy, but its underlying working mechanism remains largely unexplored. The current study uncovered the pathogenic role and underlying mechanism of a novel Smad3-dependent long noncoding RNA (lncRNA) (LRNA9884) in type 2 diabetic nephropathy (T2DN). We found that LRNA9884 was significantly upregulated in the diabetic kidney of db/db mice at the age of 8 weeks preceding the onset of microalbuminuria and was associated with the progression of diabetic renal injury. LRNA9884 was induced by advanced glycation end products and tightly regulated by Smad3, and its levels were significantly blunted in db/db mice and cells lacking Smad3. More importantly, kidney-specific silencing of LRNA9884 effectively attenuated diabetic kidney injury in db/db mice, as shown by the reduction of histological injury, albuminuria excretion, and serum creatinine. Mechanistically, we identified that LRNA9884 promoted renal inflammation-driven T2DN by triggering MCP-1 production at the transcriptional level, and its direct binding significantly enhanced the promoter activity of MCP-1. Thus, LRNA9884 is a novel Smad3-dependent lncRNA that is highly expressed in db/db mice associated with T2DN development. Targeting of LRNA9884 effectively blocked MCP-1-dependent renal inflammation, therefore suppressing the progressive diabetic renal injury in db/db mice. This study reveals that LRNA9884 may be a novel and precision therapeutic target for T2DN in the future. [ABSTRACT FROM AUTHOR]

Published
2019
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27. USMB-shMincle: a virus-free gene therapy for blocking M1/M2 polarization of tumor-associated macrophages.

Author

Xue VW, Chung JY, Tang PC, Chan AS, To TH, Chung JS, Mussal F, Lam EW, Li C, To KF, Leung KT, Lan HY, and Tang PM

Abstract

Mincle is essential for tumor-associated macrophage (TAM)-driven cancer progression and represents a potential immunotherapeutic target for cancer. Nevertheless, the lack of a specific inhibitor has largely limited its clinical translation. Here, we successfully developed a gene therapeutic strategy for silencing Mincle in a virus-free and tumor-specific manner by combining RNA interference technology with an ultrasound-microbubble-mediated gene transfer system (USMB). We identified a small hairpin RNA (shRNA) sequence shMincle that can silence not only Mincle expression but also the protumoral effector production in mouse bone marrow- and human THP-1-derived macrophages in the cancer setting in vitro . By using our well-established USMB system (USMB-shMincle), the shMincle-expressing plasmids were delivered in a tissue-specific manner into xenografts of human lung carcinoma A549 and melanoma A375 in vivo . Encouragingly, we found that USMB-shMincle effectively inhibited the protumoral phenotypes of TAMs as well as the progression of both A549 and A375 xenografts in a dose-dependent manner in mice without significant side effects. Mechanistically, we identified that USMB-shMincle markedly enhanced the anticancer M1 phenotype of TAMs in the A549 and A375 xenografts by blocking the protumoral Mincle/Syk/nuclear factor κB (NF-κB) signaling axis. Thus, USMB-shMincle may represent a clinically translatable novel and safe gene therapeutic approach for cancer treatment., Competing Interests: The authors declare no competing interests., (© 2021 The Author(s).)

Published
2021
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28. LRNA9884, a Novel Smad3-Dependent Long Noncoding RNA, Promotes Diabetic Kidney Injury in db / db Mice via Enhancing MCP-1-Dependent Renal Inflammation.

Author

Zhang YY, Tang PM, Tang PC, Xiao J, Huang XR, Yu C, Ma RCW, and Lan HY

Subjects
Animals, Chemokine CCL2 genetics, Computational Biology, Glycation End Products, Advanced pharmacology, Kidney drug effects, Male, Mice, Mice, Inbred Strains, Real-Time Polymerase Chain Reaction, Signal Transduction drug effects, Signal Transduction genetics, Smad3 Protein antagonists & inhibitors, Chemokine CCL2 metabolism, Diabetic Nephropathies metabolism, Inflammation metabolism, Kidney metabolism, RNA, Long Noncoding metabolism, Smad3 Protein metabolism
Abstract

Transforming growth factor-β/Smad3 signaling plays an important role in diabetic nephropathy, but its underlying working mechanism remains largely unexplored. The current study uncovered the pathogenic role and underlying mechanism of a novel Smad3-dependent long noncoding RNA (lncRNA) (LRNA9884) in type 2 diabetic nephropathy (T2DN). We found that LRNA9884 was significantly upregulated in the diabetic kidney of db / db mice at the age of 8 weeks preceding the onset of microalbuminuria and was associated with the progression of diabetic renal injury. LRNA9884 was induced by advanced glycation end products and tightly regulated by Smad3, and its levels were significantly blunted in db / db mice and cells lacking Smad3. More importantly, kidney-specific silencing of LRNA9884 effectively attenuated diabetic kidney injury in db / db mice, as shown by the reduction of histological injury, albuminuria excretion, and serum creatinine. Mechanistically, we identified that LRNA9884 promoted renal inflammation-driven T2DN by triggering MCP-1 production at the transcriptional level, and its direct binding significantly enhanced the promoter activity of MCP-1. Thus, LRNA9884 is a novel Smad3-dependent lncRNA that is highly expressed in db / db mice associated with T2DN development. Targeting of LRNA9884 effectively blocked MCP-1-dependent renal inflammation, therefore suppressing the progressive diabetic renal injury in db / db mice. This study reveals that LRNA9884 may be a novel and precision therapeutic target for T2DN in the future., (© 2019 by the American Diabetes Association.)

Published
2019
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