Wnt activator FOXB2 drives prostate cancer neuroendocrine differentiation

  title={Wnt activator FOXB2 drives prostate cancer neuroendocrine differentiation},
  author={Lavanya Moparthi and Giulia Pizzolato and Stefan Koch},
The Wnt signaling pathway is of paramount importance for development and disease. However, the tissue-specific regulation of Wnt pathway activity remains incompletely understood. Here we identify FOXB2, an uncharacterized forkhead box family transcription factor, as a potent activator of Wnt signaling in normal and cancer cells. Mechanistically, FOXB2 induces the non-classical Wnt ligand WNT7B, which increases TCF/LEF-dependent transcription without activating LRP6 or β-catenin. Proximity… 
Forkhead box B2 inhibits the malignant characteristics of the pancreatic cancer cell line Panc‐1 in vitro
FoxB2 has the ability to inhibit the malignant characteristics of Panc‐1 in vitro, and this work suggests that it acts as a tumor suppressor.


FOXQ1 mediates the crosstalk between TGF-β and Wnt signaling pathways in the progression of colorectal cancer
It is demonstrated that FOXQ1 plays a critical role during the tumorigenesis of colorectal cancer and is a mediator of the crosstalk between Wnt and TGF-β signaling pathways.
Role of WNT7B-induced Noncanonical Pathway in Advanced Prostate Cancer
It is suggested that AR-regulated WNT7B signaling is critical for the growth of CRPC and development of the osteoblastic bone response characteristic of advanced prostate cancer.
Forkhead Box F2 Suppresses Gastric Cancer through a Novel FOXF2-IRF2BPL-β-Catenin Signaling Axis.
FoxF2-mediated upregulation of the E3 ligase IRF2BPL drives ubiquitylation and degradation of β-catenin in gastric cancer, blunting Wnt signaling and suppressing carcinogenesis.
WNT7B mediates autocrine Wnt/β-catenin signaling and anchorage-independent growth in pancreatic adenocarcinoma
The findings indicate WNT7B can serve as a primary determinant of differential Wnt/β-catenin activation in PDAC and other cancer contexts where Wnt activation is mediated by ligand expression rather than mutations in canonical pathway members.
Analysis of Wnt Gene Expression in Prostate Cancer
It is found that WNT11 expression is elevated in hormone-independent prostate cancer cell lines and in high-grade prostatic tumors and in hormones-independent xenografts, which are consistent with a model in which androgen depletion activates W NT11-dependent signals that inhibit androgen-dependent but not androgens-independent cell growth.
FOXKs promote Wnt/β-catenin signaling by translocating DVL into the nucleus.
Wnt-11 promotes neuroendocrine-like differentiation, survival and migration of prostate cancer cells
The increased level of Wnt-11 found in prostate cancer contributes to tumour progression by promoting NED, tumour cell survival and cell migration/invasion, and may provide an opportunity for novel therapy in prostatecancer.
Wnt proteins synergize to activate β-catenin signaling
It is shown that coexpression of specific Wnt ligands synergistically activates β-catenin signaling with biological consequences, and Wnt synergy provides a general mechanism to confer increased combinatorial control over this important regulatory pathway.