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Facts about Protein LYRIC.
Promotes anchorage-independent growth of immortalized melanocytes and astrocytes which is a key component in tumor cell expansion. Promotes lung metastasis and also has an impact on bone and brain metastasis, possibly by enhancing the seeding of tumor cells into the target organ endothelium.
Mouse | |
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Gene Name: | Mtdh |
Uniprot: | Q80WJ7 |
Entrez: | 67154 |
Belongs to: |
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No superfamily |
3D3; AEG1; AEG-13D3/LYRIC; AEG1LYRIC/3D3; Astrocyte elevated gene-1 protein; LYRIC; LYRICMetastasis adhesion protein; Lysine-rich CEACAM1 co-isolated protein; Metadherin; MTDH; protein LYRIC
Mass (kDA):
63.846 kDA
Mouse | |
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Location: | 15 B3.1|15 13.98 cM |
Sequence: | 15; |
In the mammary gland, expressed at the apical surface of epithelial cells lining ducts, as well as in the mammary fat pad. Not detected in the spleen, kidney, lung, or skin; minute amounts seen in the liver. Expressed in Purkinje neurons in the early postnatal and adult cerebellum. Overexpressed in mammary tumors (at protein level).
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AEG-1/MTDH/LYRIC is an important mediator of cancer development and regulation. It regulates a broad range of essential tumor processes, according to the research of Su et al. In this review, we highlight some of the most important functions of this protein. Despite its ubiquitin-proteoglycan-binding domains, MTDH is unique among vertebrate immune systems and is associated with inflammation.
SCCHN is characterized by high rate of metastasis and mortality. MTDH plays a key role in this process by inhibiting SCCHN cell invasion and metastasis. We found that rhCCL18 increased MTDH expression, resulting in transcriptional activation of NF-kB. Furthermore, MTDH-deficient cells exhibited enhanced migration and invasion in response to CCL18 stimulation.
The role of MTDH in HCC metastasis is largely unknown, but it has been shown to be involved in tumor growth. Interestingly, MTDH is a confirmed target of miR-375, which has been found to be downregulated in sixty human HCC. This research reveals a unique pathway in the development of HCC metastasis.
MTDH is also involved in the DNA damage response, and a transgenic mouse model expressing hepatocyte-specific MTDH knockout has shown that this protein has a critical role in this process. Alb/MTDH hepatocytes were found to have reduced ROS levels and a delayed activation of CHK1 and CHK2. Moreover, endogenous MTDH is distributed throughout the nucleus, whereas the transgenic model shows mainly cytoplasmic localization.
MTDH is a coactivator and inhibitor of the p65 subunit of NF-kB. It also inhibits a variety of other genes, including the ATP-binding cassette transporter ABCC11 (MRP8), the transcription factor CP2 and CREB-binding protein. This is a summary of the various studies that support the role of MTDH in HCC.
The overexpression of AEG-1/MTDH/LYRIC inhibits glutamate uptake in gliomas. AEG-1/MTDH/LYRIC overexpression also reduces the expression of EAAT2, leading to glioma-induced neurodegeneration. Its role in cancer development is also unclear. However, the potential for therapy of LPS-related diseases and septic shock has been shown.
MTDH is an important regulator of chemoresistance. Knocking down AEG-1/MTDH/LYRIC inhibits the expression of LYRIC. This interaction also influences lyric activity, which controls FOXO3 expression and activity. Furthermore, knockdown of AEG-1/MTDH/LYRIC decreases tumor cell growth. Inhibition of AEG-1/MTDH/LYRIC decreases the expression of Gag, resulting in reduced viral infectivity. Further experiments are needed to determine whether MTDH/LYRIC regulates chemosensibility.
Molecular studies show that MTDH is a coactivator. This protein is involved in many cancer processes, including angiogenesis. Hypoxia, inflammation, and MTDH/LYRIC crosstalk can lead to tumor angiogenesis. Moreover, these three proteins can influence tumor growth and angiogenesis. They are also coactivators of NF-kB and AEG-1. However, these interactions are not conclusive.
Two new drugs from Boster Bio have been shown to inhibit MTDH activity. MTDH is a coactivator of NF-kB that facilitates translocation into the nucleus. MTDH interacts with the p65 subunit of NF-kB and promotes downstream gene expression. These compounds are promising targets for glioma cells.
These new drugs are effective against glioma by inhibiting MTDH, a critical oncogene that participates in almost every aspect of cancer progression. MTDH promotes EMT-like processes by regulating the expression of miR-130b, a small RNA involved in the regulation of the nuclear envelope. Both drugs suppress miR-130b and PPP2CA-mediated glioma cell invasion.
In experiments, U87 cells were seeded in six-well plates and cultured until confluence. At various time points, a wound was created on each monolayer by scratching the cell surface with a sterile pipette tip. Monolayers were then washed twice with PBS and incubated with DMEM without FBS. After 24 hours, photos of the healed wounds were taken using an Axiovert 200 microscope. Absorbance at 490 nm was measured and the difference between control and treatment groups was noted. All experiments were done in triplicate, unless otherwise specified.
Mutations in the PPP2CA gene cause intellectual and neurodevelopmental disorders. The protein plays a critical role in brain function and is involved in several diseases. Mutations in this gene may result in a dominant-negative effect. The treatment is a novel approach to addressing neurodevelopmental disorders. This drug is a potent and highly effective treatment for PPP2A mutations.
The role of MTDH in regulating miR-130b ceRNA expression is gaining increasing relevance. MTDH is a critical factor that controls the activity of many RNA-binding proteins, including miR-130b. MTDH regulates miR-130b expression in glioma cells. Furthermore, MTDH also acts on several other RNA-binding proteins. This means that it is one of the most important regulators of miR-130b gene expression.
MTDH is a crucial oncogene that participates in every aspect of the progression and development of cancer. In glioma cells, MTDH promotes the expression of genes that promote cell invasion, including MMP2 and MMP9. MTDH regulates miR-130b ceRNA expression and modulates many other RNA-binding proteins. This makes it an essential part of the cancer cell invasion process.
While the role of MTDH is unclear, it has been implicated in EMT in several tumor cells. MTDH overexpression promoted EMT, while knockdown reversed this effect. MTDH also promoted EMT in tongue squamous cell carcinoma cells. It is believed to promote EMT via the Wnt/PCP signaling pathway and also the p38 MAPK/SMAD7 signaling pathway. It has not yet been proven that MTDH is part of a miRNA regulation network, but it has been found to modulate miRNA function.
This peptide is also involved in regulating the expression of other miRNAs. One study has shown that miR-130b is upregulated in a number of tissues, including the intestine. This molecule has important effects on tumor cells and tumor suppressors. Boster Bio MTDH regulates miR-130b ceRNA expression and may provide an alternative method of cancer therapy.
This is the first time that miR-130b has been shown to modulate glioma cell invasion through its regulation of miRNA. Metadherin is a key player in EMT in several cancers, including glioma. In addition, it modulates the expression of glioma-related miRNAs, such as miR-130b.
The role of MTDH in prostate cancer metastasis is not well understood. It is associated with the development of prostate cancer through its suppression of MMP2 expression. However, it is not known what role MTDH plays in this process, but it may help determine how the disease progresses. In the meantime, Boster Bio MTDH regulates miR-130b ceRNA expression through its modulation of MTDH.
To examine the role of MTDH in the regulation of miR-130b ceRNA expression, the authors used stable U87 glioma cell lines. The cells were cultured in DMEM containing 1% penicillin-streptomycin. Transient transfection of MTDH, siRNAs, and miR-130b-cRNA was performed on the cultures. All experiments were performed in triplicate.
miR-130b/301b cluster are two vertebrate specific miRNA precursor genes. miR-130b is located at chr11 while miR-301b is found in chr22. The miR-130b/301b gene cluster has been characterized as having a similar seed region and processing from the 3' arm of a hairpin. In addition to MTDH, the miR-130b/301b cluster is also associated with oncogenic activity.
PMID: 15093543 by Brown D.M., et al. Metadherin, a cell surface protein in breast tumors that mediates lung metastasis.
PMID: 14980505 by Sutherland H.G.E., et al. 3D3/lyric: a novel transmembrane protein of the endoplasmic reticulum and nuclear envelope, which is also present in the nucleolus.
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