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563 results on '"Tang, Hsin-Yao"'

5. Markers of fungal translocation are elevated during post-acute sequelae of SARS-CoV-2 and induce NF-κB signaling

Author

Giron, Leila B, Peluso, Michael J, Ding, Jianyi, Kenny, Grace, Zilberstein, Netanel F, Koshy, Jane, Hong, Kai Ying, Rasmussen, Heather, Miller, Gregory E, Bishehsari, Faraz, Balk, Robert A, Moy, James N, Hoh, Rebecca, Lu, Scott, Goldman, Aaron R, Tang, Hsin-Yao, Yee, Brandon C, Chenna, Ahmed, Winslow, John W, Petropoulos, Christos J, Kelly, J Daniel, Wasse, Haimanot, Martin, Jeffrey N, Liu, Qin, Keshavarzian, Ali, Landay, Alan, Deeks, Steven G, Henrich, Timothy J, and Abdel-Mohsen, Mohamed

Subjects
Infectious Diseases, Prevention, Emerging Infectious Diseases, Lung, Biodefense, Vaccine Related, Pneumonia, 2.1 Biological and endogenous factors, Aetiology, Infection, Inflammatory and immune system, Good Health and Well Being, COVID-19, Humans, Inflammation, Lectins, C-Type, NF-kappa B, SARS-CoV-2, Syk Kinase, beta-Glucans, Post-Acute COVID-19 Syndrome, Tight junctions, Virology
Abstract

Long COVID, a type of post-acute sequelae of SARS-CoV-2 (PASC), has been associated with sustained elevated levels of immune activation and inflammation. However, the mechanisms that drive this inflammation remain unknown. Inflammation during acute coronavirus disease 2019 could be exacerbated by microbial translocation (from the gut and/or lung) to blood. Whether microbial translocation contributes to inflammation during PASC is unknown. We did not observe a significant elevation in plasma markers of bacterial translocation during PASC. However, we observed higher levels of fungal translocation - measured as β-glucan, a fungal cell wall polysaccharide - in the plasma of individuals experiencing PASC compared with those without PASC or SARS-CoV-2-negative controls. The higher β-glucan correlated with higher inflammation and elevated levels of host metabolites involved in activating N-methyl-d-aspartate receptors (such as metabolites within the tryptophan catabolism pathway) with established neurotoxic properties. Mechanistically, β-glucan can directly induce inflammation by binding to myeloid cells (via Dectin-1) and activating Syk/NF-κB signaling. Using a Dectin-1/NF-κB reporter model, we found that plasma from individuals experiencing PASC induced higher NF-κB signaling compared with plasma from negative controls. This higher NF-κB signaling was abrogated by piceatannol (Syk inhibitor). These data suggest a potential targetable mechanism linking fungal translocation and inflammation during PASC.

Published
2022

12. Stromal changes in the aged lung induce an emergence from melanoma dormancy

Author

Fane, Mitchell E., Chhabra, Yash, Alicea, Gretchen M., Maranto, Devon A., Douglass, Stephen M., Webster, Marie R., Rebecca, Vito W., Marino, Gloria E., Almeida, Filipe, Ecker, Brett L., Zabransky, Daniel J., Hüser, Laura, Beer, Thomas, Tang, Hsin-Yao, Kossenkov, Andrew, Herlyn, Meenhard, Speicher, David W., Xu, Wei, Xu, Xiaowei, Jaffee, Elizabeth M., Aguirre-Ghiso, Julio A., and Weeraratna, Ashani T.

Published
2022
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15. Expression of the αVβ3 integrin affects prostate cancer sEV cargo and density and promotes sEV pro‐tumorigenic activity in vivo through a GPI‐anchored receptor, NgR2.

Author

Verrillo, Cecilia E., Quaglia, Fabio, Shields, Christopher D., Lin, Stephen, Kossenkov, Andrew V., Tang, Hsin‐Yao, Speicher, David, Naranjo, Nicole M., Testa, Anna, Kelly, William K., Liu, Qin, Leiby, Benjamin, Musante, Luca, Sossey‐Alaoui, Khalid, Dogra, Navneet, Chen, Tzu‐Yi, Altieri, Dario C., and Languino, Lucia R.

Subjects
FOCAL adhesion kinase, EXTRACELLULAR matrix, EXTRACELLULAR vesicles, CANCER cell proliferation, TETRASPANIN
Abstract

It is known that small extracellular vesicles (sEVs) are released from cancer cells and contribute to cancer progression via crosstalk with recipient cells. We have previously reported that sEVs expressing the αVβ3 integrin, a protein upregulated in aggressive neuroendocrine prostate cancer (NEPrCa), contribute to neuroendocrine differentiation (NED) in recipient cells. Here, we examine the impact of αVβ3 expression on sEV protein content, density and function. sEVs used in this study were isolated by iodixanol density gradients and characterized by nanoparticle tracking analysis, immunoblotting and single vesicle analysis. Our proteomic profile of sEVs containing αVβ3 shows downregulation of typical effectors involved in apoptosis and necrosis and an upregulation of tumour cell survival factors compared to control sEVs. We also show that the expression of αVβ3 in sEVs causes a distinct reposition of EV markers (Alix, CD81, CD9) to a low‐density sEV subpopulation. This low‐density reposition is independent of extracellular matrix (ECM) protein interactions with sEVs. This sEV subset contains αVβ3 and an αVβ3 downstream effector, NgR2, a novel marker for NEPrCa. We show that sEVs containing αVβ3 are loaded with higher amounts of NgR2 as compared to sEVs that do not express αVβ3. Mechanistically, we demonstrate that sEVs containing NgR2 do not affect the sEV marker profile, but when injected in vivo intratumorally, they promote tumour growth and induce NED. We show that sEVs expressing NgR2 increase the activation of focal adhesion kinase (FAK), a known promoter of cancer cell proliferation, in recipient cells. We also show that NgR2 mimics the effect of sEVs containing αVβ3 since it displays increased growth of NgR2 transfectants in vivo, as compared to control cells. Overall, our results describe the changes that occur in cargo, density and functions of cancer cell‐derived sEVs containing the αVβ3 integrin and its effector, NgR2, without affecting the sEV tetraspanin profiles. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Differentially Disrupted Spinal Cord and Muscle Energy Metabolism in Spinal and Bulbar Muscular Atrophy

Author

DeBartolo, Danielle, Arnold, Frederick, Liu, Y, Molotsky, Elana, Tang, Hsin-Yao, Merry, Diane, DeBartolo, Danielle, Arnold, Frederick, Liu, Y, Molotsky, Elana, Tang, Hsin-Yao, and Merry, Diane

Abstract

Prior studies showed that polyglutamine-expanded androgen receptor (AR) is aberrantly acetylated and that deacetylation of the mutant AR by overexpression of nicotinamide adenine dinucleotide-dependent (NAD+-dependent) sirtuin 1 is protective in cell models of spinal and bulbar muscular atrophy (SBMA). Based on these observations and reduced NAD+ in muscles of SBMA mouse models, we tested the therapeutic potential of NAD+ restoration in vivo by treating postsymptomatic transgenic SBMA mice with the NAD+ precursor nicotinamide riboside (NR). NR supplementation failed to alter disease progression and had no effect on increasing NAD+ or ATP content in muscle, despite producing a modest increase of NAD+ in the spinal cords of SBMA mice. Metabolomic and proteomic profiles of SBMA quadriceps muscles indicated alterations in several important energy-related pathways that use NAD+, in addition to the NAD+ salvage pathway, which is critical for NAD+ regeneration for use in cellular energy production. We also observed decreased mRNA levels of nicotinamide riboside kinase 2 (Nmrk2), which encodes a key kinase responsible for NR phosphorylation, allowing its use by the NAD+ salvage pathway. Together, these data suggest a model in which NAD+ levels are significantly decreased in muscles of an SBMA mouse model and intransigent to NR supplementation because of decreased levels of Nmrk2.

Published
2024

18. Targeting glutamine dependence through GLS1 inhibition suppresses ARID1A-inactivated clear cell ovarian carcinoma

Author

Wu, Shuai, Fukumoto, Takeshi, Lin, Jianhuang, Nacarelli, Timothy, Wang, Yemin, Ong, Dionzie, Liu, Heng, Fatkhutdinov, Nail, Zundell, Joseph A., Karakashev, Sergey, Zhou, Wei, Schwartz, Lauren E., Tang, Hsin-Yao, Drapkin, Ronny, Liu, Qin, Huntsman, David G., Kossenkov, Andrew V., Speicher, David W., Schug, Zachary T., Van Dang, Chi, and Zhang, Rugang

Published
2021
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20. sFRP2 in the aged microenvironment drives melanoma metastasis and therapy resistance

Author

Kaur, Amanpreet, Webster, Marie R, Marchbank, Katie, Behera, Reeti, Ndoye, Abibatou, Kugel, Curtis H, Dang, Vanessa M, Appleton, Jessica, O’Connell, Michael P, Cheng, Phil, Valiga, Alexander A, Morissette, Rachel, McDonnell, Nazli B, Ferrucci, Luigi, Kossenkov, Andrew V, Meeth, Katrina, Tang, Hsin-Yao, Yin, Xiangfan, Wood, William H, Lehrmann, Elin, Becker, Kevin G, Flaherty, Keith T, Frederick, Dennie T, Wargo, Jennifer A, Cooper, Zachary A, Tetzlaff, Michael T, Hudgens, Courtney, Aird, Katherine M, Zhang, Rugang, Xu, Xiaowei, Liu, Qin, Bartlett, Edmund, Karakousis, Giorgos, Eroglu, Zeynep, Lo, Roger S, Chan, Matthew, Menzies, Alexander M, Long, Georgina V, Johnson, Douglas B, Sosman, Jeffrey, Schilling, Bastian, Schadendorf, Dirk, Speicher, David W, Bosenberg, Marcus, Ribas, Antoni, and Weeraratna, Ashani T

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Adult, Aging, Animals, Cell Line, Tumor, Culture Media, Conditioned, DNA Damage, DNA-(Apurinic or Apyrimidinic Site) Lyase, Disease Progression, Drug Resistance, Neoplasm, Fibroblasts, Humans, Indoles, Male, Melanoma, Membrane Proteins, Mice, Microphthalmia-Associated Transcription Factor, Middle Aged, Molecular Targeted Therapy, Neoplasm Metastasis, Neovascularization, Pathologic, Oxidative Stress, Phenotype, Reactive Oxygen Species, Sulfonamides, Tumor Microenvironment, Vemurafenib, Wnt Signaling Pathway, Wnt1 Protein, beta Catenin, General Science & Technology
Abstract

Cancer is a disease of ageing. Clinically, aged cancer patients tend to have a poorer prognosis than young. This may be due to accumulated cellular damage, decreases in adaptive immunity, and chronic inflammation. However, the effects of the aged microenvironment on tumour progression have been largely unexplored. Since dermal fibroblasts can have profound impacts on melanoma progression, we examined whether age-related changes in dermal fibroblasts could drive melanoma metastasis and response to targeted therapy. Here we find that aged fibroblasts secrete a Wnt antagonist, sFRP2, which activates a multi-step signalling cascade in melanoma cells that results in a decrease in β-catenin and microphthalmia-associated transcription factor (MITF), and ultimately the loss of a key redox effector, APE1. Loss of APE1 attenuates the response of melanoma cells to DNA damage induced by reactive oxygen species, rendering the cells more resistant to targeted therapy (vemurafenib). Age-related increases in sFRP2 also augment both angiogenesis and metastasis of melanoma cells. These data provide an integrated view of how fibroblasts in the aged microenvironment contribute to tumour progression, offering new possibilities for the design of therapy for the elderly.

Published
2016

24. MYC regulates fatty acid metabolism through a multigenic program in claudin-low triple negative breast cancer

Author

Casciano, Jessica C., Perry, Caroline, Cohen-Nowak, Adam J., Miller, Katelyn D., Vande Voorde, Johan, Zhang, Qifeng, Chalmers, Susan, Sandison, Mairi E., Liu, Qin, Hedley, Ann, McBryan, Tony, Tang, Hsin-Yao, Gorman, Nicole, Beer, Thomas, Speicher, David W., Adams, Peter D., Liu, Xuefeng, Schlegel, Richard, McCarron, John G., Wakelam, Michael J. O., Gottlieb, Eyal, Kossenkov, Andrew V., and Schug, Zachary T.

Published
2020
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45. Molecular Basis for Maternal Inheritance of Human Mitochondrial DNA

Author

Lee, William, primary, Zamudio-Ochoa, Angelica, additional, Buchel, Gina, additional, Podlesniy, Petar, additional, Marti Gutierrez, Nuria, additional, Puigros, Margalida, additional, Calderon, Anna, additional, Koski, Amy, additional, Tang, Hsin-Yao, additional, Li, Li, additional, Trullas, Ramon, additional, Mitalipov, Shoukhrat, additional, and Temiakov, Dmitry, additional

Published
2023
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47. Supplementary Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2

Author

Alicea, Gretchen M., primary, Rebecca, Vito W., primary, Goldman, Aaron R., primary, Fane, Mitchell E., primary, Douglass, Stephen M., primary, Behera, Reeti, primary, Webster, Marie R., primary, Kugel, Curtis H., primary, Ecker, Brett L., primary, Caino, M. Cecilia, primary, Kossenkov, Andrew V., primary, Tang, Hsin-Yao, primary, Frederick, Dennie T., primary, Flaherty, Keith T., primary, Xu, Xiaowei, primary, Liu, Qin, primary, Gabrilovich, Dmitry I., primary, Herlyn, Meenhard, primary, Blair, Ian A., primary, Schug, Zachary T., primary, Speicher, David W., primary, and Weeraratna, Ashani T., primary

Published
2023
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48. Supplementary Movie 1 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2

Author

Alicea, Gretchen M., primary, Rebecca, Vito W., primary, Goldman, Aaron R., primary, Fane, Mitchell E., primary, Douglass, Stephen M., primary, Behera, Reeti, primary, Webster, Marie R., primary, Kugel, Curtis H., primary, Ecker, Brett L., primary, Caino, M. Cecilia, primary, Kossenkov, Andrew V., primary, Tang, Hsin-Yao, primary, Frederick, Dennie T., primary, Flaherty, Keith T., primary, Xu, Xiaowei, primary, Liu, Qin, primary, Gabrilovich, Dmitry I., primary, Herlyn, Meenhard, primary, Blair, Ian A., primary, Schug, Zachary T., primary, Speicher, David W., primary, and Weeraratna, Ashani T., primary

Published
2023
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49. Supplementary Movie 2 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2

Author

Alicea, Gretchen M., primary, Rebecca, Vito W., primary, Goldman, Aaron R., primary, Fane, Mitchell E., primary, Douglass, Stephen M., primary, Behera, Reeti, primary, Webster, Marie R., primary, Kugel, Curtis H., primary, Ecker, Brett L., primary, Caino, M. Cecilia, primary, Kossenkov, Andrew V., primary, Tang, Hsin-Yao, primary, Frederick, Dennie T., primary, Flaherty, Keith T., primary, Xu, Xiaowei, primary, Liu, Qin, primary, Gabrilovich, Dmitry I., primary, Herlyn, Meenhard, primary, Blair, Ian A., primary, Schug, Zachary T., primary, Speicher, David W., primary, and Weeraratna, Ashani T., primary

Published
2023
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50. Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2

Author

Alicea, Gretchen M., primary, Rebecca, Vito W., primary, Goldman, Aaron R., primary, Fane, Mitchell E., primary, Douglass, Stephen M., primary, Behera, Reeti, primary, Webster, Marie R., primary, Kugel, Curtis H., primary, Ecker, Brett L., primary, Caino, M. Cecilia, primary, Kossenkov, Andrew V., primary, Tang, Hsin-Yao, primary, Frederick, Dennie T., primary, Flaherty, Keith T., primary, Xu, Xiaowei, primary, Liu, Qin, primary, Gabrilovich, Dmitry I., primary, Herlyn, Meenhard, primary, Blair, Ian A., primary, Schug, Zachary T., primary, Speicher, David W., primary, and Weeraratna, Ashani T., primary

Published
2023
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