양경원 교수

Abstract Apoptosis inhibitor of macrophage (AIM) modulates the signaling in inflammatory responses, including infection, cancer, or other immune diseases. Recent studies suggest that like interleukin-10 (IL-10), AIM is involved in alternatively activated (M2) macrophage polarization. We aimed to understand whether and how AIM is involved in IL-10-induced inhibition of inflammasome activation and resolution of inflammation. First, we demonstrated that IL-10 induced increases in mRNA and protein e

Abstract The interplay between apoptotic cancer cells and the tumor microenvironment modulates cancer progression and metastasis. Cancer-associated fibroblasts (CAFs) play a crucial role in promoting these events through paracrine communication. Here, we demonstrate that conditioned medium (CM) from lung CAFs exposed to apoptotic cancer cells suppresses TGF-β1-induced migration and invasion of cancer cells and CAFs. Direct exposure of CAFs to apoptotic 344SQ cells (ApoSQ) inhibited CAF migration

Previously, we demonstrated that growth arrest-specific protein 6 (Gas6)/Axl or Mer signaling inhibited the transforming growth factor (TGF)-β1-induced epithelial–mesenchymal transition (EMT) in lung epithelial cells. Hepatocyte growth factor (HGF) has also been shown to inhibit TGF-β1-induced changes in EMT markers. Here, we examined whether Gas6 signaling can induce the production of HGF and c-Met in lung alveolar epithelial cells to mediate the inhibition of EMT and to inhibit the migration a

Cell death within the tumor microenvironment (TME) plays a crucial role in controlling cancer by influencing the balance of tumor-specific immunity. Cancer-associated fibroblasts (CAFs) significantly contribute to tumor progression through paracrine mechanisms. We found that reprogramming of CAFs by apoptotic cancer cells suppresses tumor volume and lung metastasis. Here, we investigated the mechanisms by which the interaction between apoptotic lung cancer cells and CAFs hinders tumor growth. Ex

Introduction Growth arrest-specific 6 (Gas6) protein signaling plays a critical role in maintaining immune homeostasis and regulating inflammation. However, novel mechanisms for modulating macrophage activity through the Gas6 axis are being identified. Gas6 enhances the production of apoptosis inhibitor of macrophages (AIM), a protein with potent anti-inflammatory properties. This study investigates whether Gas6-induced AIM suppresses acute lung injury (ALI) in mice by modulating key inflammator

This study was to investigate the correlation between pain, disability and quality of life among adolescents and office workers with neck and shoulder pain.

T cells and reduced accumulation of regulatory T cells within the tumor. Notably, these effects were abolished by either depletion of WISP-1 from the CM or pharmacological inhibition of STAT1 following recombinant WISP-1 administration. Collectively, our findings identify the WISP-1-integrin α5β3-STAT1 axis as a novel therapeutic target for TAM reprogramming and tumor suppression in lung cancer.

Recent studies highlight the critical role of cancer-associated fibroblasts (CAFs)- tumor-associated macrophages (TAMs) interactions in tumorigenesis. In prior work, we demonstrated that the interaction between CAFs and apoptotic cancer cells can inhibit tumor growth and metastasis. However, the molecular mechanisms underlying the crosstalk between CAFs reprogrammed by apoptotic cancer cells and TAMs are incompletely understood. In this study, we show, using immunohistochemistry in primary tumor

Abstract The interplay between apoptotic cancer cells and the tumor microenvironment (TME) modulates cancer progression and metastasis. Cancer-associated fibroblasts (CAFs) play a crucial role in promoting these events through paracrine communication. In the present study, we investigated how the interaction of CAFs with apoptotic lung cancer cells modulates migration and invasion of cancer cells and CAFs. CAFs isolated from the lung tumors of Kras-mutant (KrasLA1) mice and ultraviolet-irradiate