Transcriptional Regulation of Wnt/β-Catenin Pathway in Colorectal Cancer

Abstract

The Wnt/β-catenin signaling pathway exerts integral roles in embryogenesis and adult homeostasis. Aberrant activation of the pathway is implicated in growth-associated diseases and cancers, especially as a key driver in the initiation and progression of colorectal cancer (CRC). Loss or inactivation of Adenomatous polyposis coli (APC) results in constitutive activation of Wnt/β-catenin signaling, which is considered as an initiating event in the development of CRC. Increased Wnt/β-catenin signaling is observed in virtually all CRC patients, underscoring the importance of this pathway for therapeutic intervention. Prior studies have deciphered the regulatory networks required for the cytoplasmic stabilisation or degradation of the Wnt pathway effector, β-catenin. However, the mechanism whereby nuclear β-catenin drives or inhibits expression of Wnt target genes is more diverse and less well characterised. Here, we describe a brief synopsis of the core canonical Wnt pathway components, set the spotlight on nuclear mediators and highlight the emerging role of chromatin regulators as modulators of β-catenin-dependent transcription activity and oncogenic output.

SNHG9 promotes Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

“…The canonical Wnt signaling pathway participates in normal functioning of diverse physiological processes. However, its abnormal aberrant activation results in the development and progression of cancer 17 , 40 , 50 , 51 . We identified miR23a-5p binding sites on Wnt3a using the RNA hybrid database and showed reduced luciferase activity on HB cell lines co-transfected with Wnt3aWT and miR-23a-mimics.…”

SNHG9 Promotes the Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

“…The canonical Wnt signaling pathway participate in normal functioning of diverse physiological processes however, it`s abnormal aberrant activation resulting in development and progression of cancer (1,13,43,44). We identi ed miR23a-5p binding sites on Wnt3a using RNA hybrid database and showed reduced luciferase activity on HB cell lines co-transfected with Wnt3aWT and miR-23a-mimics.…”

ENO1 Inhibits Apoptosis and Promotes Cell Invasion and Proliferation in Malignant Melanoma

“…Wnt/β-catenin canonical signaling has a vital function melanoma apoptosis, invasion, migration, proliferation, and differentiation. [20][21][22][23] The core component of the Wnt/β-catenin pathway, β-catenin, has an important function in tumor progression. 24 c-Myc can induce tumor cells to transition from the G1 phase to the S phase, thereby promoting cell proliferation.…”