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- Table of Contents
1 Citations 8 Q&As
Facts about Securin.
Throughout the mitosis, it blocks Separase/ESPL1 function, preventing the proteolysis of the cohesin complex and the subsequent segregation of the chromosomes. At the onset of anaphase, it's ubiquitinated, conducting to its destruction and to the liberation of ESPL1.
Human | |
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Gene Name: | PTTG1 |
Uniprot: | O95997 |
Entrez: | 9232 |
Belongs to: |
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securin family |
EAP1MGC126883; ESP1-associated protein 1; Esp1-associated protein; hPTTG; pituitary tumor-transforming 1; Pituitary tumor-transforming gene 1 protein; PTTGMGC138276; securin; Tumor-transforming protein 1; TUTR1HPTTG
Mass (kDA):
22.024 kDA
Human | |
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Location: | 5q33.3 |
Sequence: | 5; NC_000005.10 (160421855..160428744) |
Expressed at low level in most tissues, except in adult testis, where it is highly expressed. Overexpressed in many patients suffering from pituitary adenomas, primary epithelial neoplasias, and esophageal cancer.
Cytoplasm. Nucleus.
This is the best PTTG1 marker in hepatocellular cancer. This protein regulates cell senescence, migration, invasion, and metastasis. Its usefulness in cancer research reaches all scientists around the world. In this article, you will learn more about PTTG1's uses in cancer research.
PTTG1, one of 17 gene-signature combinations that have been proven to predict prognosis for different types and metastasis, is one of them. Multiple studies have shown PTTG1 excess is associated with tumor proliferation and invasiveness. Conversely, PTTG1 overexpression is associated with tumor proliferation and invasiveness. However, downregulation of PTTG1 increases survival rates and reduces cancer risk. Using a biomarker of PTTG1, we might be able to identify a new biomarker against hepatocellular carcinoma.
PTTG1 has been identified as a novel oncogene. It was found to be overexpressed within many human tumors. It is not clear if PTTG1 is clinically relevant in NSCLC. We assessed its expression status in NSCLC using publicly available GEO databases and immunohistochemistry. We also compared PTTG1 levels in NSCLC to those of normal lung samples.
In a recent study we identified five TME -related IRGs which were significant predictors of RFS/OS in LIHC. These genes were FABP6, CD4, EREG, and PRF1. These genes were examined and revealed that the expression levels of PTTG1 were significantly related to the stage of patients with LIHC. Several of these genes were previously thought to be associated with high-risk or poor-risk patients.
Interestingly, PTTG1 gene expression was positively correlated in glioma and pan-kidney cancer cohorts. It was also associated to higher levels of natural killer lymphocyte and cytotoxic Lymphocyte infiltration in BLCA. These results suggest PTTG1 might be a biomarker to detect hepatocellular carcinoma.
Besides microarray data, other data were also analyzed. These data include a KEGG pathway analysis as well as gene expression databases. We used STRING and KEGG pathway enrichment tools to construct a PPI network. These data helped us identify genes that were upregulated or downregulated in PTTG1. Based on the enrichment analysis of KEGG pathways, several of these genes were identified by us as hub genes.
A large-scale study in China found that PTTG1 significantly upregulates a number of genes. MT1X was discovered to be the hub genes among them. It was found that five genes are associated with HCC diagnosis. The association with HCC was not seen for the other three MT1s.
In contrast, PTTG1 has no role in the progression of hepatocellular carcinoma in a study of pituitary cancer. Although PTTG1 is not thought to be directly connected with the disease progression it is thought that the existence of PTTG1 antibodies may indicate a malignant status. Therefore, we have to look for ways to identify a biomarker of PTTG1 to aid in detecting cancer patients.
hPTTG1 regulates the process by which breast cancer cells colonize lung tissue in mice. It stimulates the metastasis and growth of breast cancer cells by activating the GEFh2 signalling pathway. This axis has been implicated recently in breast cancer metastasis, despite being poorly understood. Evidence has been found linking hPTTG1 & hGEF–h2.
Although PTTG1 has been implicated in the master regulator of tumor metastasisis in previous studies, their exact mechanisms are still unknown. Additionally, it is possible that PTTG1 works in concert with FoxM1 to regulate cell movement and invasion. However, more research is needed to discover how FoxM1 & PTTG1 regulate these processes.
Some human cancers, like lung cancer and melanoma have high levels of PTTG1. Its excessive expression promotes tumorigenesis and increases tumor-associated angiogenesis. These functions are thought to contribute to the carcinogenesis and DNA repair. In addition, the overexpression of PTTG1 increases tumor metastasis and cell growth.
PTTG1 has a role in senescence. However it is also a key regulator to cell transforming activation, which is necessary for cell retraction. Furthermore, hPTTG1 has been shown to regulate cell motility by transactivating cyclin D3 and p21. Although the exact mechanism of this interaction remains elusive, it is believed to be critical for controlling cell polarity, invasion and metastasis.
The GEF/h2/RhoA signalling pathway is used to examine the role that hPTTG1 plays in cancer metastasis. This protein regulates cell motility and acts as a cytoskeleton regulator. Further studies are needed to determine how the hPTTG1 protein contributes to cancer metastasis.
PTTG1 has been linked to various types of cancer. High levels of hPTTG1 found in tumors were associated increased grade, invasiveness and vascularity. It also has transforming activity. Soft agar assays show that hPTTG1 overexpression in cancer cells results is larger colonies than controls. In contrast, knocking down hPTTG1 inhibits soft agar colony formation.
The inhibition of hPTTG1 reduces cancer cell proliferation and inhibits its progression. Depletion and inhibition of hPTTG1 can reduce cancer cell proliferation as well as inhibit tumour metastasis. Overexpression of hPTTG1 also inhibits E-Cadherin (a protein that controls cell movement). These findings are crucial for cancer research as well as the development of therapies.
Orthotopic injections with MDA-MB-231 cell cells inhibit the growth of primary tumours for 6 weeks. The tumour grew slower after this time. Moreover, hPTTG1 knockdown inhibits tumour growth in a spontaneous metastatic mouse model. This finding supports that hPTTG1 plays an important role in metastasis.
GEFh2 regulates transcriptional control of PTTG1 in order to prevent cancer. It regulates cell migration, invasion, as well as senescence. It also influences apoptosis. Cancer cells may be able, by using this gene, to escape their prognosis.
It is still unclear whether PTTG1 may be used to treat HCC. PTTG1 is important, but many patients will have poor outcomes with standard therapies for these cancers. It is known to promote metastasis and proliferation, and to be useful for clinical diagnosis and prognosis. Studies have shown PTTG1 might also be a candidate in targeted therapy for other types of cancer.
The authors conducted a study that identified 445 differentially expressed genes (DEGs) in HCC tissues. To identify significant gene sets with enriched gene set, the authors used two GEO datasets. These genes were further studied using coexpression analysis, blue modules, and GSEA analyses. The phenotype-related gene sets resulting from the analysis included upregulated, under-expressed, and both gene sets.
Using KEGG pathway analysis and GO enrichment, DEGs were associated with 147 pathways in HCC. The enriched modules contained metabolic processes, cell cycle, oxidation/reduction, and P450 -associated pathways. DEGs are involved in metabolic processes as well as PPAR signaling and fatty acids degradation. These findings suggest that PTTG1 may be a potential therapeutic target in HCC.
PTTG1 is also responsible for regulating the expression of p21. Higher levels p21 reduce the development of pituitary tumours. Interestingly, removing p21 resulted in a decrease in growth and proliferation. Overexpression of PTTG1 in tumors causes them to express p21. This can lead to cell senescence. These results suggest that PTTG1 may inhibit p21-mediated tumor growth.
Although the CDC6 genes is highly expressed in most types of cancers, it is also found in aggressive prostate cancers and in a subset not-small cell lung cancers. It may be able to provide effective treatment for advanced cancer patients, even though the role of CDC6 is still unclear. To understand the role of CDC6 as it relates to the progression of HCC, further research is needed.
This study used gene-chips and RNAseq data to identify genes that are highly expressed during HCC. The pPTTG1 gene is expressed at higher levels than the controls in TCGA–GTEx. The prognosis of HCC victims in both cohorts is affected by the expression levels of PTTG1. However, survival rates in the LIHC cohort are less consistent with PTTG1 expression, suggesting that PTTG1 might not be a viable therapeutic target.
PMID: 9811450 by Dominguez A., et al. hPTTG, a human homologue of rat PTTG, is overexpressed in hematopoietic neoplasms. Evidence for a transcriptional activation function of hPTTG.
PMID: 10393434 by Kakar S.S., et al. Molecular cloning and characterization of the tumor transforming gene (TUTR1): a novel gene in human tumorigenesis.
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