NUPR1

Official Full Name

nuclear protein 1, transcriptional regulator

Organism

Homo sapiens

GeneID

26471

Background

Enables DNA binding activity and transcription coactivator activity. Involved in several processes, including negative regulation of programmed cell death; positive regulation of oxidative phosphorylation; and regulation of catabolic process. Acts upstream of or within negative regulation of cell cycle. Located in intercellular bridge; nucleoplasm; and perinuclear region of cytoplasm. Part of protein-DNA complex. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

P8; COM1;

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Detailed Information

Transcription regulator nuclear protein-1 (Nupr1) is a cell stress protein. Different external pressures and cell microenvironment can affect its expression and mediate its nuclear entry to regulate the transcription of various genes. This directly or indirectly triggers different intracellular signaling pathways and produces corresponding cytological effects, participating in the occurrence and development of tumors and non-tumor diseases.

Figure 1. A schematic illustrating the role of Nupr1 in METH-induced apoptosis and autophagy in neuronal cells. （Xu, X., et al. 2017）

The Role of Nupr1 in the Occurrence and Development of Neoplastic Diseases

In neoplastic diseases, Nupr1 can produce different effects in different tumor microenvironments, which can both promote and inhibit the progress of tumors, such as the same double-edged sword. In pancreatic cancer, tumor cells have high expression of Nupr1 (while high expression is not found in pancreatic fibrocysts and normal pancreatic cells), Nupr1 changes the level of DNA methylation by inhibiting the expression of DNA methyltransferase 1, inhibits Kirsten rat sarcoma virus proto-oncogene-induced cell death, and promotes pancreatic intraepithelial neoplasia. In breast cancer, the high expression of Nupr1 is an important factor for the poor prognosis of early breast cancer patients, and Nupr1 can promote the growth of human breast cancer cells in the inoculated organs, which has a certain relationship with its metastasis.

Nupr1 is moderately expressed in normal human lung tissue. Down-regulating its expression can not only reduce the proliferation of non-small cell lung cancer, in vitro clone formation and tumorigenicity in nude mice, but also block the cell cycle at G0/G1 period. In addition, it can promote cell death by regulating the autophagy tide. In medullary thyroid tumors, the expression level of Nupr1 is directly related to lymph node metastasis, and 24.8% of patients with higher Nupr1 expression relapsed. In prostate cancer cells, overexpression of Nupr1 can increase the sensitivity of cells to cycloglitazone and may act as a tumor suppressor.

Nupr1 and Non-neoplastic Diseases

In the acute phase of pancreatitis, Nupr1 expression is up-regulated, and P8 expression is also increased during pancreatic gland development and regeneration after resection. The researchers studied the response of the immune system of the spleen cells of the Knpr1 gene knockout rats and wild-type rats in acute pancreatitis, and found that Nu-pr1 may maintain the balance of the immune response by limiting apoptosis. At the same time, they also found that Nupr1 is involved in the cell's antioxidant defense mechanism.

In the psychic system, Nupr1 is a key gene for oxidative stress in astrocytes, and up-regulation of Nupr1mRNA expression can enhance the tolerance of cells to stress injury. Similarly, in human osteoarthritis cartilage, Nupr1 expression is higher than normal cartilage, and IL-1β stimulation can induce chondrocyte Nupr1mRNA expression to increase, which may be a new IL-1β regulated matrix metalloproteinase molecule pathway. Quantitative PCR method was used to detect the level of Nupr1 in mouse ovary, testis, liver and pancreas tissues, and it was found that Nupr1 expression could be detected in these tissues, and the level of Nupr1mRNA in ovarian and testicular tissues was much higher than that of pancreas and liver. Therefore, it is speculated that it plays an important role in ovarian maturation and the maintenance of normal testicular sperm count.

Nupr1 and the mechanism of diabetes and its complications are also the focus of research. Researchers found that in type Ⅱ diabetes, Nupr1 can affect the expression of heat shock protein 70, change the body's sensitivity to insulin, and thus affect blood sugar levels. Reducing the expression of Nupr1 can obviously increase the body's sensitivity to insulin, this research result provides a new idea for the treatment of type II diabetes. In an animal model of diabetic nephropathy treated with streptozotocin, induced by endothelin, angiotensin and glucagon, Nupr1 expression is up-regulated, which in turn stimulates mesangial cell hypertrophy.

References:

Xu, X., et al. (2017) Nupr1 Modulates Methamphetamine-Induced Dopaminergic Neuronal Apoptosis and Autophagy through CHOP-Trib3-Mediated Endoplasmic Reticulum Stress Signaling Pathway. Frontiers in Molecular Neuroscience,10: p. 203.
Cai, D. , Huang, E. , Luo, B. , Yang, Y. , Zhang, F. , & Liu, C. , et al. (2016). Nupr1/chop signal axis is involved in mitochondrion-related endothelial cell apoptosis induced by methamphetamine. Cell Death & Disease, 7(3), e2161.
Marie-Sophie, N. , Ionela-Mariana, N. , Olga, O. , Valery, B. , Julie, L. , & Maria, F. , et al. (2018). A novel role for Nupr1 in the keratinocyte stress response to uv oxidized phospholipids. Free Radical Biology & Medicine, 120, S38-.

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