LncRNA CCAL is up-regulated in colorectal cancer (CRC) tissues and high CCAL level is associated with poor overall survival and a worse response to adjuvant chemotherapy. Further studies reveal that CCAL promotes CRC progression by targeting activator protein 2α (AP-2α), which in turn activates Wnt/β-catenin pathway. Moreover, CCAL induces multidrug resistance (MDR) through activating Wnt/β-catenin signaling by suppressing AP-2α and further up-regulating MDR1/P-gp expression. In addition, histone H3 methylation and deacetylases contribute to the upregulation of CCAL in CRC (1).
|LncRNA||tissue||cancer type||expression level||oncogene/suppress gene||pathway||binding gene/factor||associated gene/factor||proliferation||apoptosis||migration||EMT||invasion||metastasis||prognosis||tag||PMID|
|0||CCAL||colorectum||colorectal cancer||up||onco||Wnt/β-catenin pathway+||MDR1/P-gp+,AP-2α-||-||chemotherapy resistance||25994219|