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Authors = Max Kam-Kwan Chan

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23 pages, 916 KiB  
Review
LncRNA-Dependent Mechanisms of Transforming Growth Factor-β: From Tissue Fibrosis to Cancer Progression
by Philip Chiu-Tsun Tang, Ying-Ying Zhang, Jane Siu-Fan Li, Max Kam-Kwan Chan, Jiaoyi Chen, Ying Tang, Yiming Zhou, Dongmei Zhang, Kam-Tong Leung, Ka-Fai To, Sydney Chi-Wai Tang, Hui-Yao Lan and Patrick Ming-Kuen Tang
Non-Coding RNA 2022, 8(3), 36; https://doi.org/10.3390/ncrna8030036 - 25 May 2022
Cited by 15 | Viewed by 4301
Abstract
Transforming growth factor-β (TGF-β) is a crucial pathogenic mediator of inflammatory diseases. In tissue fibrosis, TGF-β regulates the pathogenic activity of infiltrated immunocytes and promotes extracellular matrix production via de novo myofibroblast generation and kidney cell activation. In cancer, TGF-β promotes cancer invasion [...] Read more.
Transforming growth factor-β (TGF-β) is a crucial pathogenic mediator of inflammatory diseases. In tissue fibrosis, TGF-β regulates the pathogenic activity of infiltrated immunocytes and promotes extracellular matrix production via de novo myofibroblast generation and kidney cell activation. In cancer, TGF-β promotes cancer invasion and metastasis by enhancing the stemness and epithelial mesenchymal transition of cancer cells. However, TGF-β is highly pleiotropic in both tissue fibrosis and cancers, and thus, direct targeting of TGF-β may also block its protective anti-inflammatory and tumor-suppressive effects, resulting in undesirable outcomes. Increasing evidence suggests the involvement of long non-coding RNAs (lncRNAs) in TGF-β-driven tissue fibrosis and cancer progression with a high cell-type and disease specificity, serving as an ideal target for therapeutic development. In this review, the mechanism and translational potential of TGF-β-associated lncRNAs in tissue fibrosis and cancer will be discussed. Full article
(This article belongs to the Section Long Non-Coding RNA)
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18 pages, 16222 KiB  
Review
TGF-β Signaling: From Tissue Fibrosis to Tumor Microenvironment
by Jeff Yat-Fai Chung, Max Kam-Kwan Chan, Jane Siu-Fan Li, Alex Siu-Wing Chan, Philip Chiu-Tsun Tang, Kam-Tong Leung, Ka-Fai To, Hui-Yao Lan and Patrick Ming-Kuen Tang
Int. J. Mol. Sci. 2021, 22(14), 7575; https://doi.org/10.3390/ijms22147575 - 15 Jul 2021
Cited by 132 | Viewed by 23418
Abstract
Transforming growth factor-β (TGF-β) signaling triggers diverse biological actions in inflammatory diseases. In tissue fibrosis, it acts as a key pathogenic regulator for promoting immunoregulation via controlling the activation, proliferation, and apoptosis of immunocytes. In cancer, it plays a critical role in tumor [...] Read more.
Transforming growth factor-β (TGF-β) signaling triggers diverse biological actions in inflammatory diseases. In tissue fibrosis, it acts as a key pathogenic regulator for promoting immunoregulation via controlling the activation, proliferation, and apoptosis of immunocytes. In cancer, it plays a critical role in tumor microenvironment (TME) for accelerating invasion, metastasis, angiogenesis, and immunosuppression. Increasing evidence suggest a pleiotropic nature of TGF-β signaling as a critical pathway for generating fibrotic TME, which contains numerous cancer-associated fibroblasts (CAFs), extracellular matrix proteins, and remodeling enzymes. Its pathogenic roles and working mechanisms in tumorigenesis are still largely unclear. Importantly, recent studies successfully demonstrated the clinical implications of fibrotic TME in cancer. This review systematically summarized the latest updates and discoveries of TGF-β signaling in the fibrotic TME. Full article
(This article belongs to the Special Issue Molecular Research in Medical Genetics)
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19 pages, 913 KiB  
Review
The Emerging Role of Innate Immunity in Chronic Kidney Diseases
by Philip Chiu-Tsun Tang, Ying-Ying Zhang, Max Kam-Kwan Chan, Winson Wing-Yin Lam, Jeff Yat-Fai Chung, Wei Kang, Ka-Fai To, Hui-Yao Lan and Patrick Ming-Kuen Tang
Int. J. Mol. Sci. 2020, 21(11), 4018; https://doi.org/10.3390/ijms21114018 - 4 Jun 2020
Cited by 41 | Viewed by 6242
Abstract
Renal fibrosis is a common fate of chronic kidney diseases. Emerging studies suggest that unsolved inflammation will progressively transit into tissue fibrosis that finally results in an irreversible end-stage renal disease (ESRD). Renal inflammation recruits and activates immunocytes, which largely promotes tissue scarring [...] Read more.
Renal fibrosis is a common fate of chronic kidney diseases. Emerging studies suggest that unsolved inflammation will progressively transit into tissue fibrosis that finally results in an irreversible end-stage renal disease (ESRD). Renal inflammation recruits and activates immunocytes, which largely promotes tissue scarring of the diseased kidney. Importantly, studies have suggested a crucial role of innate immunity in the pathologic basis of kidney diseases. This review provides an update of both clinical and experimental information, focused on how innate immune signaling contributes to renal fibrogenesis. A better understanding of the underlying mechanisms may uncover a novel therapeutic strategy for ESRD. Full article
(This article belongs to the Special Issue Immune Cell Mediated Tissue Regeneration)
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