Abstract
There is no radical cure for all cancer types. The most frequently used therapies are surgical treatment, radiotherapy and chemotherapy. However, recrudescence, radiation resistance and chemotherapy resistance are the most challenging issues in clinical practice. To address these issues, they should be further studied at the molecular level, and the signaling pathways involved represent a promising avenue for this research. In the present review, we mainly discuss the components and mechanisms of activation of the Notch and Wnt signaling pathways, and we summarize the recent research efforts on these two pathways in different cancers. We also evaluate the ideal drugs that could target these two signaling pathways for cancer therapy, summarize alterations in the Notch and Wnt signaling pathways in cancer, and discuss potential signaling inhibitors as effective drugs for cancer therapy.
Highlights
There is no radical cure for all cancer types
We mainly focus on the Notch and Wnt signaling pathways to summarize their mechanism of activation, their role in tumorigenesis and their potential as targets for cancer therapy
The activation was shown to be regulated via proteolysis by metalloprotease, tumor necrosis factor-α-converting enzyme (TACE) and γ-secretase [21,22]
Summary
Liu et al [129] reported that LKB1, a tumor suppressor, could inhibit the Wnt signal pathway through increasing GSK3β activity, causing low expression of β-catenin. SOX10, was reported to inhibit the epithelial to mesenchymal transition (EMT) and stemness ability in ESCC cells, by competing with TCF4 to bind β-catenin [130] From these studies, we may conclude that Wnt signal pathway plays an important role in ESCC. Studies have shown that targeting the components of Wnt signal pathway could inhibit the malignant activity of ESCC cell lines, indicating it is a potential treatment of ESCC. Recent studies showed that LRP5/6, closely related membrane receptors for the Wnt signaling pathway, can be targeted by antibodies for further treatment in cancer [154,155]. ICG-001 inhibited β-catenin activity in nucleus by disrupting β-catenin /CBP interaction [168] (Fig. 2)
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