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Filamin A interacting protein 1-like (FILIP1L) is a multifunctional, tumor-suppressor-like protein that regulates cell migration, invasion, apoptosis, angiogenesis, and cell proliferation, primarily in the context of cancer[1][2][3][4]. It inhibits canonical WNT/β-catenin signaling and suppresses the epithelial-mesenchymal transition (EMT), thereby reducing metastasis and chemoresistance[2][3]. FILIP1L is downregulated in numerous cancer types, often due to promoter methylation, and its reduced expression is associated with poor prognosis, enhanced tumor progression, increased chemoresistance, and metastatic potential[1][2][3][4][5]. FILIP1L may also localize to mitochondria and play a role in cytoskeletal remodeling[4]. It does not fall into classic receptor, enzyme, transporter, or transcription factor classes, but is considered a promising molecular target for cancer therapy and a prognostic biomarker[1][2][3][4].
Promotes β-catenin degradation and suppresses WNT/β-catenin signaling[2][3]; Suppresses MMP9 expression and activity, limiting invasion/metastasis[3]; Induces cell cycle arrest and apoptosis; Inhibits vascular endothelial growth factor (VEGF)-mediated angiogenesis[1]
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