DCC

Official Full Name

DCC netrin 1 receptor

Organism

Homo sapiens

GeneID

1630

Background

This gene encodes a netrin 1 receptor. The transmembrane protein is a member of the immunoglobulin superfamily of cell adhesion molecules, and mediates axon guidance of neuronal growth cones towards sources of netrin 1 ligand. The cytoplasmic tail interacts with the tyrosine kinases Src and focal adhesion kinase (FAK, also known as PTK2) to mediate axon attraction. The protein partially localizes to lipid rafts, and induces apoptosis in the absence of ligand. The protein functions as a tumor suppressor, and is frequently mutated or downregulated in colorectal cancer and esophageal carcinoma. [provided by RefSeq, Oct 2009]

Synonyms

CRC18; CRCR1; MRMV1; HGPPS2; IGDCC1; NTN1R1;

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Detailed Information

The DCC (Deleted in Colorectal Cancer) gene is a crucial player in various cellular processes, including cell migration, axon guidance, and neurogenesis. It belongs to the immunoglobulin superfamily and functions as a tumor suppressor by inhibiting cell migration, invasion, and angiogenesis. The DCC gene is frequently deleted in CRC, leading to its loss of function and promoting tumor progression.

Function And Structure of The DCC Gene

The DCC gene encodes a protein of the same name, which is a transmembrane protein with a molecular weight of approximately 180 kDa. The protein contains an extracellular domain, a transmembrane domain, and a cytoplasmic domain. The extracellular domain contains a fibronectin-like domain, a cysteine-rich domain, and a mucin-like domain. The cytoplasmic domain interacts with various proteins to regulate signaling pathways.

The function of the DCC gene is diverse and complex. In neurons, it serves as a guidance receptor for axon growth and guidance during development. In epithelial cells, it plays a role in cell-cell adhesion and differentiation. In cancer cells, it acts as a tumor suppressor by regulating cell migration and invasion. The DCC gene code a transmembrane protein that interacts with various signaling molecules, including those involved in Wnt, RTK, and Notch signaling pathways. Activation of these pathways can lead to the disruption of cell polarity, promotion of cell migration, and increased cell proliferation, which are important for tumorigenesis and cancer progression. Inhibition of DCC function can result in the unregulated activation of these signaling pathways, contributing to the development of colorectal cancer. Therefore, understanding the DCC-regulated signaling pathways may provide insights into the development and progression of colorectal cancer and suggest potential therapeutic targets for its treatment.

Figure 1. Schematic representation of the known signaling pathways induced by DCC.

DCC And Singal Pathway

The DCC-related signaling pathways involve multiple mechanisms that control cell behavior. One of the key pathways is the RTK/RAS/PI3K/AKT pathway. In normal cells, DCC interacts with integrins, which activates the RTK/RAS/PI3K/AKT signaling cascade. This results in the phosphorylation of various downstream targets, including GSK3β, FOXO, and CLASP2, leading to cell adhesion, differentiation, and apoptosis. In CRC cells, the loss of DCC results in the dysregulation of this pathway, leading to uncontrolled cell proliferation, migration, and invasion. Another important pathway is the Wnt/β-catenin pathway. DCC interacts with Frizzled receptors and inhibits the activation of β-catenin, which otherwise leads to the transcription of genes involved in cell proliferation and tumorigenesis. In the absence of DCC, the Wnt/β-catenin pathway is constitutively activated, promoting CRC development.

DCC And Cancer

The DCC gene plays a crucial role in tumor development, particularly in the colon and rectum. This gene is responsible for encoding a protein called DCC receptor, which helps to regulate cell growth and differentiation. In normal conditions, the DCC gene prevents unwanted cell proliferation and ensures tissue homeostasis. However, when the DCC gene is mutated or deleted, it leads to uncontrolled cell growth and increased tumor susceptibility. The function of the DCC receptor is to interact with various signaling pathways within the cell, which ultimately govern cell fate. When the DCC gene is altered, the receptor's activity is disrupted, causing cells to lose their normal growth control mechanisms. This results in the development of colon cancer, as well as other cancers involving the gastrointestinal tract.

Reference:

Gao, Ruijuan et al. "Macrophage-derived netrin-1 drives adrenergic nerve-associated lung fibrosis." The Journal of clinical investigation vol. 131,1 (2021): e136542. doi:10.1172/JCI136542

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