Since the initial discovery of the oncogenic activity of WNT1 in mouse mammary glands, our appreciation for the complex roles for WNT signalling pathways in cancer has increased dramatically. WNTs and their downstream effectors regulate various processes that are important for cancer progression, including tumour initiation, tumour growth, cell senescence, cell death, differentiation and metastasis. Although WNT signalling pathways have been difficult to target, improved drug-discovery platforms and new technologies have facilitated the discovery of agents that can alter WNT signalling in preclinical models, thus setting the stage for clinical trials in humans.

WNT signalling pathways as therapeutic targets in cancer

Caught up in a Wnt storm: Wnt signaling in cancer.

Wnt5a signaling directly affects cell motility and invasion of metastatic melanoma.

β-Catenin can function as an oncogene when it is translocated to the nucleus, binds to T cell factor or lymphoid enhancer factor family members, and transactivates its target genes. In this study, we demonstrate that cyclin D1 is one of the targets of β-catenin in breast cancer cells. Transactivation of β-catenin correlated significantly with cyclin D1 expression both in eight breast cell lines in vitro and in 123 patient samples. More importantly, we found that high β-catenin activity significantly correlated with poor prognosis of the patients and was a strong and independent prognostic factor in breast cancer. Our studies, therefore, indicated that β-catenin can be involved in breast cancer formation and/or progression and may serve as a target for breast cancer therapy.

https://www.pnas.org/content/pnas/97/8/4262.full.pdf

β-Catenin, a novel prognostic marker for breast cancer: Its roles in cyclin D1 expression and cancer progression

Wnt signaling is a highly conserved signaling pathway that plays a critical role in controlling embryonic and organ development, as well as cancer progression. Genome-wide sequencing and gene expression profile analyses have demonstrated that Wnt signaling is involved mainly in the processes of breast cancer proliferation and metastasis. The most recent studies have indicated that Wnt signaling is also crucial in breast cancer immune microenvironment regulation, stemness maintenance, therapeutic resistance, phenotype shaping, etc. Wnt/β-Catenin, Wnt–planar cell polarity (PCP), and Wnt–Ca2+ signaling are three well-established Wnt signaling pathways that share overlapping components and play different roles in breast cancer progression. In this review, we summarize the main findings concerning the relationship between Wnt signaling and breast cancer and provide an overview of existing mechanisms, challenges, and potential opportunities for advancing the therapy and diagnosis of breast cancer.

/pdf/wnt-signaling-in-breast-cancer-biological-mechanisms-1vnui54avm.pdf

Wnt signaling in breast cancer: biological mechanisms, challenges and opportunities

Wnt genes are involved in mouse mammary cancer, but their role in human cancer is unknown. Human Wnt5a was cloned from a placental cDNA library and used to assess expression by ribonuclease protection and in situ hybridization in human breast cell lines and in normal, benign, and malignant breast tissues. Human Wnt5a shows over 99% homology at amino acid level with mouse Wnt5a, and 90% with Xenopus Wnt5a. It was expressed only at low levels in breast cell lines and normal breast tissue. Benign proliferations and invasive cancer respectively showed 10-fold and 4-fold higher Wnt5a than normal breast tissues. The greater up-regulation in benign conditions suggests a role in aberrant differentiation. In situ hybridization localized the signal to the epithelial component. Wnt5a is the first member of the Wnt family to demonstrate overexpression in human breast cancer. It was not associated with factors known to affect breast cancer prognosis such as lymph node status or epidermal growth factor receptor status.

/pdf/wnt5a-cloning-expression-and-up-regulation-in-human-primary-218mce3hta.pdf

Wnt5a cloning, expression, and up-regulation in human primary breast cancers.

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Wnt5a cloning, expression, and up-regulation in human primary breast cancers.