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11. EPITHELIAL TO MESENCHYMAL TRANSITION (EMT) AND PD-1/PD-L1 SIGNALING PROVIDE RECIPROCAL FEEDBACK IN RENAL CELL CARCINOMA PROGRESSION WITH IMPLICATIONS FOR IMMUNOTHERAPY RESPONSE

Author

Wainstein, Matthew D., primary, McGue, Jake, additional, Robinson, Tyler, additional, Mehra, Rohit, additional, Salami, Simpa S., additional, Frankel, Tim, additional, Udager, Aaron, additional, Keller, Evan T., additional, May, Allison M., additional, and Jiang, Jonathan, additional

Published
2024
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13. Dysregulated Ribosome Biogenesis Is a Targetable Vulnerability in Triple-Negative Breast Cancer: MRPS27 as a Key Mediator of the Stemness-inhibitory Effect of Lovastatin

Author

Zheng, Chanjuan, primary, Yao, Hui, additional, Lu, Lu, additional, Li, Hongqi, additional, Zhou, Lei, additional, He, Xueyan, additional, Xu, Xi, additional, Xia, Hongzhuo, additional, Ding, Siyu, additional, Yang, Yiyuan, additional, Wang, Xinyu, additional, Wu, Muyao, additional, Xue, Lian, additional, Chen, Sisi, additional, Peng, Xiaojun, additional, Cheng, Zhongyi, additional, Wang, Yian, additional, He, Guangchun, additional, Fu, Shujun, additional, Keller, Evan T., additional, Liu, Suling, additional, Jiang, Yi-zhou, additional, and Deng, Xiyun, additional

Published
2024
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19. Polarization of Prostate Cancer-associated Macrophages Is Induced by Milk Fat Globule-EGF Factor 8 (MFG-E8)-mediated Efferocytosis*

Author

Soki, Fabiana N, Koh, Amy J, Jones, Jacqueline D, Kim, Yeo Won, Dai, Jinlu, Keller, Evan T, Pienta, Kenneth J, Atabai, Kamran, Roca, Hernan, and McCauley, Laurie K

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Cancer, Urologic Diseases, Prostate Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Antigens, Surface, Cell Line, Tumor, Flow Cytometry, Macrophages, Male, Mice, Mice, Inbred C57BL, Milk Proteins, Prostatic Neoplasms, Real-Time Polymerase Chain Reaction, Bone, Bone Marrow, Macrophage, Phagocytosis, Alternative Activation, MFG-E8, Skeletal Metastasis, Tumor-associated Macrophages, Efferocytosis, Chemical Sciences, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Chemical sciences
Abstract

Tumor cells secrete factors that modulate macrophage activation and polarization into M2 type tumor-associated macrophages, which promote tumor growth, progression, and metastasis. The mechanisms that mediate this polarization are not clear. Macrophages are phagocytic cells that participate in the clearance of apoptotic cells, a process known as efferocytosis. Milk fat globule- EGF factor 8 (MFG-E8) is a bridge protein that facilitates efferocytosis and is associated with suppression of proinflammatory responses. This study investigated the hypothesis that MFG-E8-mediated efferocytosis promotes M2 polarization. Tissue and serum exosomes from prostate cancer patients presented higher levels of MFG-E8 compared with controls, a novel finding in human prostate cancer. Coculture of macrophages with apoptotic cancer cells increased efferocytosis, elevated MFG-E8 protein expression levels, and induced macrophage polarization into an alternatively activated M2 phenotype. Administration of antibody against MFG-E8 significantly attenuated the increase in M2 polarization. Inhibition of STAT3 phosphorylation using the inhibitor Stattic decreased efferocytosis and M2 macrophage polarization in vitro, with a correlating increase in SOCS3 protein expression. Moreover, MFG-E8 knockdown tumor cells cultured with wild-type or MFG-E8-deficient macrophages resulted in increased SOCS3 expression with decreased STAT3 activation. This suggests that SOCS3 and phospho-STAT3 act in an inversely dependent manner when stimulated by MFG-E8 and efferocytosis. These results uncover a unique role of efferocytosis via MFG-E8 as a mechanism for macrophage polarization into tumor-promoting M2 cells.

Published
2014

23. MT1-MMP-dependent control of skeletal stem cell commitment via a β1-integrin/YAP/TAZ signaling axis.

Author

Tang, Yi, Rowe, R Grant, Botvinick, Elliot L, Kurup, Abhishek, Putnam, Andrew J, Seiki, Motoharu, Weaver, Valerie M, Keller, Evan T, Goldstein, Steven, Dai, Jinlu, Begun, Dana, Saunders, Thomas, and Weiss, Stephen J

Subjects
Bone Marrow Cells, Cells, Cultured, Extracellular Matrix, Cell Nucleus, Mesenchymal Stem Cells, Animals, Mice, Inbred C57BL, Mice, Transgenic, Humans, Mice, Adaptor Proteins, Signal Transducing, Cell Cycle Proteins, Phosphoproteins, Transcription Factors, Signal Transduction, Cell Shape, Cell Lineage, Osteogenesis, Chondrogenesis, Phenotype, Adipogenesis, Matrix Metalloproteinase 14, Transcriptional Activation, Stem Cell Niche, Gene Knock-In Techniques, Proteolysis, Integrin beta1, Regenerative Medicine, Stem Cell Research, Stem Cell Research - Nonembryonic - Non-Human, Rare Diseases, 2.1 Biological and endogenous factors, Developmental Biology, Biological Sciences, Medical and Health Sciences
Abstract

In vitro, topographical and biophysical cues arising from the extracellular matrix (ECM) direct skeletal stem cell (SSC) commitment and differentiation. However, the mechanisms by which the SSC-ECM interface is regulated and the outcome of such interactions on stem cell fate in vivo remain unknown. Here we demonstrate that conditional deletion of the membrane-anchored metalloproteinase MT1-MMP (Mmp14) in mesenchymal progenitors, but not in committed osteoblasts, redirects SSC fate decisions from osteogenesis to adipo- and chondrogenesis. By effecting ECM remodeling, MT1-MMP regulates stem cell shape, thereby activating a β1-integrin/RhoGTPase signaling cascade and triggering the nuclear localization of the transcriptional coactivators YAP and TAZ, which serve to control SSC lineage commitment. These data identify a critical MT1-MMP/integrin/YAP/TAZ axis operative in the stem cell niche that oversees SSC fate determination.

Published
2013

29. Apoptosis-induced CXCL5 accelerates inflammation and growth of prostate tumor metastases in bone

Author

Roca, Hernan, Jones, Jacqueline D., Purica, Marta C., Weidner, Savannah, Koh, Amy J., Kuo, Robert, Wilkinson, John E., Wang, Yugang, Daignault-Newton, Stephanie, Pienta, Kenneth J., Morgan, Todd M., Keller, Evan T., Nor, Jacques E., Shea, Lonnie D., and McCauley, Laurie K.

Subjects
Apoptosis -- Analysis, Macrophages -- Growth -- Analysis, Cytokines -- Growth -- Analysis, Inflammation -- Development and progression -- Analysis, Prostate cancer -- Development and progression -- Analysis, Cancer metastasis -- Development and progression -- Analysis, Health care industry
Abstract

During tumor progression, immune system phagocytes continually clear apoptotic cancer cells in a process known as efferocytosis. However, the impact of efferocytosis in metastatic tumor growth is unknown. In this study, we observed that macrophage-driven efferocytosis of prostate cancer cells in vitro induced the expression of proinflammatory cytokines such as CXCL5 by activating Stat3 and NF-[kappa]B(p65) signaling. Administration of a dimerizer ligand (AP20187) triggered apoptosis in 2 in vivo syngeneic models of bone tumor growth in which apoptosis-inducible prostate cancer cells were either coimplanted with vertebral bodies, or inoculated in the tibiae of immunocompetent mice. Induction of 2 pulses of apoptosis correlated with increased infiltration of inflammatory cells and accelerated tumor growth in the bone. Apoptosis-induced tumors displayed elevated expression of the proinflammatory cytokine CXCL5. Likewise, CXCL5-deficient mice had reduced tumor progression. Peripheral blood monocytes isolated from patients with bone metastasis of prostate cancer were more efferocytic compared with normal controls, and CXCL5 serum levels were higher in metastatic prostate cancer patients relative to patients with localized prostate cancer or controls. Altogether, these findings suggest that the myeloid phagocytic clearance of apoptotic cancer cells accelerates CXCL5 -mediated inflammation and tumor growth in bone, pointing to CXCL5 as a potential target for cancer therapeutics., Introduction The most common site of prostate cancer metastasis is bone, with an incidence of 65%-80% in patients with advanced disease (1). Once cancer cells spread to bone, they significantly [...]

Published
2018
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50. Supplementary Video S3 from Fyn Is Downstream of the HGF/MET Signaling Axis and Affects Cellular Shape and Tropism in PC3 Cells

Author

Jensen, Ana R., primary, David, Saito Y., primary, Liao, Chuanhong, primary, Dai, Jinlu, primary, Keller, Evan T., primary, Al-Ahmadie, Hikmat, primary, Dakin-Haché, Kelly, primary, Usatyuk, Peter, primary, Sievert, Margarit F., primary, Paner, Gladell P., primary, Yala, Soheil, primary, Cervantes, Gustavo M., primary, Natarajan, Viswanathan, primary, Salgia, Ravi, primary, and Posadas, Edwin M., primary

Published
2023
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