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1.
J Genet Genomics ; 51(10): 997-1006, 2024 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-38885836

RESUMEN

Phospholipase D (PLD) lipid-signaling enzyme superfamily has been widely implicated in various human malignancies, but its role and underlying mechanism remain unclear in nasopharyngeal carcinoma (NPC). Here, we analyze the expressions of 6 PLD family members between 87 NPC and 10 control samples through transcriptome analysis. Our findings reveal a notable upregulation of PLD1 in both NPC tumors and cell lines, correlating with worse disease-free and overall survival in NPC patients. Functional assays further elucidate the oncogenic role of PLD1, demonstrating its pivotal promotion of critical tumorigenic processes such as cell proliferation and migration in vitro, as well as tumor growth in vivo. Notably, our study uncovers a positive feedback loop between PLD1 and the NF-κB signaling pathway to render NPC progression. Specifically, PLD1 enhances NF-κB activity by facilitating the phosphorylation and nuclear translocation of RELA, which in turn binds to the promoter of PLD1, augmenting its expression. Moreover, RELA overexpression markedly rescues the inhibitory effects in PLD1-depleted NPC cells. Importantly, the application of the PLD1 inhibitor, VU0155069, substantially inhibits NPC tumorigenesis in a patient-derived xenograft model. Together, our findings identify PLD1/NF-κB signaling as a positive feedback loop with promising therapeutic and prognostic potential in NPC.


Asunto(s)
Carcinogénesis , Proliferación Celular , Retroalimentación Fisiológica , FN-kappa B , Carcinoma Nasofaríngeo , Neoplasias Nasofaríngeas , Fosfolipasa D , Transducción de Señal , Humanos , Fosfolipasa D/genética , Fosfolipasa D/metabolismo , Carcinoma Nasofaríngeo/genética , Carcinoma Nasofaríngeo/patología , Carcinoma Nasofaríngeo/metabolismo , Transducción de Señal/genética , FN-kappa B/metabolismo , FN-kappa B/genética , Neoplasias Nasofaríngeas/genética , Neoplasias Nasofaríngeas/patología , Neoplasias Nasofaríngeas/metabolismo , Línea Celular Tumoral , Carcinogénesis/genética , Carcinogénesis/patología , Animales , Ratones , Proliferación Celular/genética , Regulación Neoplásica de la Expresión Génica , Factor de Transcripción ReIA/metabolismo , Factor de Transcripción ReIA/genética , Movimiento Celular/genética , Femenino
2.
Int J Med Sci ; 21(1): 27-36, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38164347

RESUMEN

Prokineticin 1 (PROK1) is a secreted protein involved in a range of physiological activities such as cell proliferation, migration, angiogenesis, and neuronal cell proliferation. Emerging evidences show that PROK1/PROK receptors (PROKRs) are expressed by trophoblasts, and decidual stroma cells at the maternal-fetal interface. PROK1 plays a critical role in successful pregnancy establishment by regulating the decidualization, implantation and placental development. Dysregulation of prokineticin signaling has been described in certain pathological states associated with pregnancy, including pre-eclampsia, recurrent miscarriage and fetal growth restriction. In this review, the expression and pleiotropic roles of PROK1 under physiological and pathological pregnancy conditions are discussed.


Asunto(s)
Hormonas Gastrointestinales , Preeclampsia , Factor de Crecimiento Endotelial Vascular Derivado de Glándula Endocrina , Embarazo , Femenino , Humanos , Placenta/metabolismo , Factor de Crecimiento Endotelial Vascular Derivado de Glándula Endocrina/genética , Factor de Crecimiento Endotelial Vascular Derivado de Glándula Endocrina/metabolismo , Transducción de Señal/genética , Trofoblastos , Preeclampsia/genética , Hormonas Gastrointestinales/genética , Hormonas Gastrointestinales/metabolismo
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