LncRNA MEG3 Inhibits the Epithelial-mesenchymal Transition of Bladder Cancer Cells through the Snail/E-cadherin Axis

MEG3, a #lncRNA, suppresses #EpithelialMesenchymalTransition in #BladderCancer by binding Snail to prevent #Ecadherin repression and inhibiting ERK/JNK/P38 signaling, reducing invasion and migration—highlighting its promise as a therapeutic target.

Read: doi.org/10.1007/s115...

LncRNA MEG3 Inhibits the Epithelial-mesenchymal Transition of Bladder Cancer Cells through the Snail/E-cadherin Axis - Current Medical Science Objective This study aimed to investigate the role of the long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in the epithelial-mesenchymal transition (EMT) of bladder cancer cells and the…

This study reveals that #lncRNA #Maternally expressed gene 3 (MEG3) suppresses #EpithelialMesenchymalTransition by modulating #Ecadherin via Snail/#MAPK regulation, positioning MEG3 as a potential #therapeutic target for #BladderCancer. #medsky

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Excited to share our latest pre-print “Soluble E-cadherin Drives Brain Metastasis in Inflammatory Breast Cancer” led by the outstanding Xiaoding Hu, an instructor in my lab. #Breastcancer #Brainmetastasis #IBC #Ecadherin #ReactiveAstrocytes #CXCR2

👉 biorxiv.org/content/10.110…

The transcriptomic architecture of common cancers reflects synthetic lethal interactions - Nature Genetics Tumor cells upregulate compensatory buffering genes following tumor suppressor loss. These genes may represent new synthetic lethal partners that could be harnessed therapeutically.

Uncovering synthetic lethal vulnerabilities across cancers. Upregulation of #TWIST1/2, #VIM, and integrin components ( #ITGB5, #ITGAV, #FERMT2 ) constitutes a synthetic lethal buffering mechanism that preserves tumor fitness despite #CDH1 #Ecadherin loss #lobular #DGC
www.nature.com/articles/s41...