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Wnt1 inducible signalling pathway protein-2 (WISP‑2/CCN5): roles and regulation in human cancers (review)
Jiafu Ji1, Shuqin Jia2, Ke Ji2
1Department of Gastro-enterological Cancers, Peking University Cancer Hospital, Beijing, P.R. China.
Abstract:
Wnt1 inducible signalling pathway protein-2 (WISP‑2), also known as CCN5, CT58, CTGF-L, CTGF-3, HICP and Cop1, is one of the 3 WNT1 inducible proteins that belongs to the CCN family. This family of members has been shown to play multiple roles in a number of pathophysiological processes, including cell proliferation, adhesion, wound healing, extracellular matrix regulation, epithelial-mesenchymal transition, angiogenesis, fibrosis, skeletal development and embryo implantation. Recent results suggest that WISP-2 is relevant to tumorigenesis and malignant transformation, particularly in breast cancer, colorectal cancer and hepatocarcinoma. Notably, its roles in cancer appear to vary depending on cell/tumour type and the microenvironment. The striking difference in the structure of WISP-2 in comparison with the other 2 family members may contribute to its difference in functions, which leads to the hypothesis that WISP-2 may act as a dominant-negative regulator of other CCN family members. In the present review, we summarise the roles, regulation and underlying mechanism of WISP-2 in human cancers.
Insights
Wnt1 inducible signalling pathway protein-2 (WISP-2) is involved in various cellular processes and human cancers. Its unique structure suggests it may regulate other CCN family members, impacting tumor development.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Wnt1 inducible signalling pathway protein-2 (WISP-2), also known as CCN5, is a member of the CCN family.
- CCN proteins regulate diverse cellular functions including proliferation, adhesion, wound healing, and fibrosis.
- WISP-2 has emerged as a significant factor in tumorigenesis across various cancers.
Purpose of the Study:
- To review the roles, regulation, and mechanisms of WISP-2 in human cancers.
- To explore the differential functions of WISP-2 compared to other CCN family members.
- To investigate the potential of WISP-2 as a dominant-negative regulator in cancer.
Main Methods:
- Literature review of existing studies on WISP-2.
- Analysis of WISP-2's structural differences within the CCN family.
- Synthesis of data on WISP-2's involvement in breast cancer, colorectal cancer, and hepatocarcinoma.
Main Results:
- WISP-2 plays varied roles in cancer depending on tumor type and microenvironment.
- Structural distinctions in WISP-2 suggest unique functional capabilities.
- Evidence supports WISP-2's potential role as a dominant-negative regulator of CCN family members.
Conclusions:
- WISP-2's complex roles in cancer necessitate further investigation.
- Understanding WISP-2 regulation and mechanisms is crucial for cancer therapy.
- WISP-2's unique structure and regulatory potential offer insights into cancer progression.
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