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Int J Mol Sci ; 25(8)2024 Apr 16.
Artículo en Inglés | MEDLINE | ID: mdl-38673975

RESUMEN

Previously, we reported that epidermal growth factor-like module-containing mucin-like hormone receptor-like 1 (EMR1/ADGRE1) is abnormally expressed in colon cancer (CC) and is a risk factor for lymph node metastasis (LNM) and poor recurrence-free survival in patients with abundant tumor-associated macrophages (TAMs). However, the signaling pathways associated with EMR1 expression in CC progression remain unclear. In this study, we aimed to explore the role of EMR1 and its signaling interactions with macrophages in CC progression. Spatial transcriptomics of pT3 microsatellite unstable CC tissues revealed heightened Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling in EMR1-HL CC with LNM compared to EMR1-N CC without LNM. Through in vitro coculture of CC cells with macrophages, EMR1 expression by CC cells was found to be induced by TAMs, ultimately interacting with upregulated JAK/STAT signaling, increasing cell proliferation, migration, and motility, and reducing apoptosis. JAK2/STAT3 inhibition decreased the levels of EMR1, JAK2, STAT1, and STAT3, significantly impeded the proliferation, migration, and mobility of cells, and increased the apoptosis of EMR1+ CC cells compared to their EMR1KO counterparts. Overall, TAMs-induced EMR1 upregulation in CC cells may promote LNM and CC progression via JAK2/STAT1,3 signaling upregulation. This study provides further insights into the molecular mechanisms involving macrophages and intracellular EMR1 expression in CC progression, suggesting its clinical significance and offering potential interventions to enhance patient outcomes.


Asunto(s)
Neoplasias del Colon , Janus Quinasa 2 , Transducción de Señal , Macrófagos Asociados a Tumores , Humanos , Macrófagos Asociados a Tumores/metabolismo , Macrófagos Asociados a Tumores/patología , Janus Quinasa 2/metabolismo , Janus Quinasa 2/genética , Neoplasias del Colon/patología , Neoplasias del Colon/metabolismo , Neoplasias del Colon/genética , Regulación Neoplásica de la Expresión Génica , Progresión de la Enfermedad , Regulación hacia Arriba , Proliferación Celular , Línea Celular Tumoral , Movimiento Celular/genética , Factor de Transcripción STAT1/metabolismo , Factor de Transcripción STAT1/genética , Factor de Transcripción STAT3/metabolismo , Factor de Transcripción STAT3/genética , Apoptosis/genética
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