NES

Official Full Name

nestin

Organism

Homo sapiens

GeneID

10763

Background

This gene encodes a member of the intermediate filament protein family and is expressed primarily in nerve cells. [provided by RefSeq, Sep 2011]

Synonyms

Nbla00170;

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Detailed Information

The Nestin (NES) protein, also known as nestin, was first discovered in rat embryonic neural tube cells by Hockfield and Mckay in 1985. When the neuronal precursor cells are differentiated, the nestin protein gradually disappears, and the nestin protein is considered to be a marker of neural precursor cells. In 1990, Lendahl et al. cloned a gene encoding the nestin protein. The gene structure and the intermediate filament protein gene have similar characteristics, and the middle segment α-helix structure of the encoded protein has 16% to 29% homology with the other five types of intermediate filament proteins. However, its protein has a shorter N-terminus and a longer C-terminus, and its distribution in cells is distinct from that of the other five classes of intermediate filament proteins, so it is named as class VI intermediate filament protein.

Nestin protein is not only expressed as a neural precursor cell marker in the nervous system, but also expressed in other tissues and cells, such as pancreas and liver formation during embryogenesis, angiogenesis, endothelial cells, skeletal muscle cells, epidermal basal cells, and Damaged astrocytes, etc. When these cells are divided, the nestin protein stops expressing. Intensive research has found that nestin protein is abnormally expressed in some malignant tumors, such as cerebral glioma, ependymoma, malignant melanoma and leukemia.

Nestin's Features

As an intermediate filament protein, Nestin undoubtedly has the function of maintaining the normal morphology of neural progenitor cells. The cytoskeleton containing Nestin may increase the elasticity and flexibility of nerve cells, which is essential for developmental processes. However, Nestin cannot assemble into the intermediate filament independently, and must rely on the coexisting vimentin to assemble the intermediate filaments in the neural precursor cells to play the role of the cytoskeleton. Furthermore, the breakdown of Vimentin during mitosis appears to be a unique feature of cells expressing Nestin, and Vimentin remains undecomposed throughout mitosis as Nestin expression declines. Studies suggest that non-filamentous Vimentin microparticles are precursors of intermediate filaments that are rapidly transported between different cytoplasmic compartments along microtubules. In addition, Nestin has a high distribution in neurites and its growing population, suggesting that it may be involved in the establishment of the link between neurons and target cells after mitosis. Since Nestin is distributed in the hippocampus and is related to learning and memory, it is believed that Nestin may participate in learning and memory.

Figure 1. Nestin overexpression in hepatocellular carcinomas (HCC) and cholangiocarcinomas is linked with p53 mutations and poor prognosis. (Tschaharganeh, D., et al. 2014)

Nestin and Disease

The mechanism of nestin protein expression in leukemia cells has not been reported, but in liver cancer, breast cancer and lung cancer, nestin protein is directly involved in the regulation of signal pathways involved in tumor cell proliferation. It has been reported that P53, Wnt/β-catenin signaling pathway and Akt-GSK3β-Rb signaling pathway are different in leukemia, and these changes may be associated with leukemia or worsening of patients. Studies have shown that nestin protein may act as a tumor stem cell marker, such as to further study the mechanism of action of nestin protein in cell signaling pathway, or to provide new ideas for understanding tumor cells. In vitro experiments have shown that in breast cancer, P53 deficiency is associated with high expression of nestin.

The expression of Nestin protein not only has important theoretical significance in cell molecular biology, but also researchers have detected nestin protein expression in clinical patients with acute lymphoma leukemia (ALL). In ALL patients, nestin+ cells are involved in the construction of protective niche for leukemia-propagating cells (LPCs), which promote LPCs to develop resistance and protect LPCs from chemotherapeutic agents. Currently, LPCs protective niche is found only in ALL patients, but no other malignant hematological tumors have been reported. Among them, the conversion of nestin to α-SMA is a key step for the ripening of the niche. In vitro experiments have shown that interference with nestin protein expression can disrupt the formation of this niche and attenuate the resistance of LPCs.

References:

Tschaharganeh, D. , Xue, W. , Calvisi, D. , Evert, M. , Michurina, T. , & Dow, L. , et al. (2014). P53-dependent nestin regulation links tumor suppression to cellular plasticity in liver cancer. Cell, 158(3), 579-592.
Angelino, C. . (2018). The biological role of nestin(+)-cells in physiological and pathological cardiovascular remodeling. Frontiers in Cell and Developmental Biology, 6, 15-.
Nakatomi, M. , Quispe-Salcedo, A. , Sakaguchi, M. , Ida-Yonemochi, H. , Okano, H. , & Ohshima, H. . (2018). Nestin expression is differently regulated between odontoblasts and the subodontoblastic layer in mice. Histochemistry and Cell Biology.

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