Abstract
Collagen triple helix repeat containing-1 (CTHRC1) has been identified as cancer-related protein. CTHRC1 expresses mainly in adventitial fibroblasts and neointimal smooth muscle cells of balloon-injured vessels and promotes cell migration and tissue repair in response to injury. CTHRC1 plays a pivotal role in some pathophysiological processes, including increasing bone mass, preventing myelination, and reversing collagen synthesis in many tumor cells. The ascended expression of CTHRC1 is related to tumorigenesis, proliferation, invasion, and metastasis in various human malignancies, including gastric cancer, pancreatic cancer, hepatocellular carcinoma, keloid, breast cancer, colorectal cancer, epithelial ovarian cancer, esophageal squamous cell carcinoma, cervical cancer, non-small-cell lung carcinoma, and melanoma. And molecules that regulate the expression of CTHRC1 include miRNAs, lncRNAs, WAIF1, and DPAGT1. Many reports have pointed that CTHRC1 could exert different effects through several signaling pathways such as TGF-β, Wnt, integrin β/FAK, Src/FAK, MEK/ERK, PI3K/AKT/ERK, HIF-1α, and PKC-δ/ERK signaling pathways. As a participant in tissue remodeling or immune response, CTHRC1 may promote early-stage cancer. Several recent studies have identified CTHRC1 as an effectual prognostic biomarker for predicting tumor recurrence or metastasis. It is worth noting that CTHRC1 has different cellular localization and mechanisms of action in different cells and different microenvironments. In this article, we focus on the advances in the signaling pathways mediated by CTHRC1 in tumors.
Highlights
Collagen triple helix repeat containing-1 (CTHRC1), an extracellular matrix (ECM) protein, was identified in the screening of differentially expressed sequences between balloon injury and normal arteries
CTHRC1 is abnormally expressed in several solid tumors, especially in gastric cancer, pancreatic cancer, hepatocellular carcinoma, keloid, breast cancer, colorectal cancer (CRC), epithelial ovarian cancer, esophageal squamous cell carcinoma (ESCC), cervical cancer, non-small-cell lung carcinoma (NSCLC), melanoma, and so on [11, 21,22,23,24,25,26,27,28,29,30,31]
CTHRC1 has no inhibitory effect on transforming growth factor-β (TGF-β) signaling in endothelial cells [67]. These results indicate that the regulation of TGF-β by CTHRC1 may play a role in other interstitial cells of the tumor microenvironment and that this regulation is cell type-specific
Summary
Collagen triple helix repeat containing-1 (CTHRC1), an extracellular matrix (ECM) protein, was identified in the screening of differentially expressed sequences between balloon injury and normal arteries. CTHRC1 increases the activity of collagen promoter through binding to ligands and could contribute to vascular remodeling by limiting collagen matrix deposition and promoting cell migration [4]. CTHRC1 promotes the recruitment of M2 macrophages and regulates TGF-β and Notch pathways to accelerate wound healing in a mouse model of acute wound healing [5]. CTHRC1 may promote IL-1β-induced apoptosis of chondrocytes by activating the JNK1/2 pathway [8]. The anti-inflammatory effect of CTHRC1 expressed on activated synovial cells was found in a collagen antibody-induced arthritis model [9]. A remarkable effect is that the high expression of CTHRC1 promotes tumorigenesis and development through positive regulation of tumor spread, invasion, migration, adhesion, and metastasis. CTHRC1 exerts its effects through several signaling pathways such as Mediators of Inflammation
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