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Review
. 2020 May 20;25(10):2380.
doi: 10.3390/molecules25102380.

Ras and Wnt Interaction Contribute in Prostate Cancer Bone Metastasis

Shian-Ren Lin  1 , Ntlotlang Mokgautsi  2 , Yen-Nien Liu  1   2
Affiliations
Review

Ras and Wnt Interaction Contribute in Prostate Cancer Bone Metastasis

Shian-Ren Lin et al. Molecules. .

Abstract

Prostate cancer (PCa) is one of the most prevalent and malignant cancer types in men, which causes more than three-hundred thousand cancer death each year. At late stage of PCa progression, bone marrow is the most often metastatic site that constitutes almost 70% of metastatic cases of the PCa population. However, the characteristic for the osteo-philic property of PCa is still puzzling. Recent studies reported that the Wnt and Ras signaling pathways are pivotal in bone metastasis and that take parts in different cytological changes, but their crosstalk is not well studied. In this review, we focused on interactions between the Wnt and Ras signaling pathways during each stage of bone metastasis and present the fate of those interactions. This review contributes insights that can guide other researchers by unveiling more details with regard to bone metastasis and might also help in finding potential therapeutic regimens for preventing PCa bone metastasis.

Keywords: Bone metastasis; Cross reaction; Prostate cancer; Ras; Wnt.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Molecular mechanism of bone metastasis in prostate cancer. Signaling regulators of (A) the nuclear factor (NF)-κB, transforming growth factor (TGF)-β, and (B) phosphatidylinositol-3-kinase (PI3K)/Akt signaling cascade whose is involved in bone metastasis of prostate cancer and which acts as promoters are labeled in gray and inhibitors are in black.
Figure 2
Figure 2
Diagram of Ras/Wnt interactions during prostate cancer (PCa) bone metastasis. The crosstalk from Ras to Wnt is marked in blue and vice versa in red.
See this image and copyright information in PMC

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