MTDH

Metadherin, also known as protein LYRIC or astrocyte elevated gene-1 protein (AEG-1) is a is_associated_with::protein that in humans is encoded by the MTDH is_associated_with::gene.

Function
AEG-1 is involved in HIF-1alpha mediated is_associated_with::angiogenesis. AEG-1 also interacts with is_associated_with::SND1 and involved in is_associated_with::RNA-induced silencing complex (RISC) and plays very important role in RISC and miRNA functions.

AEG-1 induces an oncogene called Late SV40 factor (LSF/is_associated_with::TFCP2) which is involved in is_associated_with::thymidylate synthase (TS) induction and DNA biosynthesis synthesis. Late SV40 factor (LSF/TFCP2) enhances angiogenesis by transcriptionally up-regulating matrix metalloproteinase-9 (is_associated_with::MMP9).

Clinical significance
AEG-1 acts as an is_associated_with::oncogene in melanoma, malignant glioma, breast cancer and hepatocellular carcinoma. It is highly expressed in these cancers and helps in progression and development of these cancers. It is induced by c-Myc oncogene and plays very important role in anchorage independent growth of cancer cells.

Elevated expression of the metastasis gene metadherin (MTDH), which is overexpressed in more than 40% of is_associated_with::breast cancers, is associated with poor clinical outcomes. MTDH has a dual role in promoting metastatic seeding and enhancing chemoresistance. MTDH is therefore a potential therapeutic target for enhancing is_associated_with::chemotherapy and reducing metastasis.

LSF/TFCP2 plays multifaceted role in chemo resistance, EMT, allergic response, inflammation and Alzheimer’s disease.

AEG-1 controls many hallmarks of oncogenes and cancer. AEG-1/MTDH induces hepato steatosis in mouse liver. The MTDH knockdown by artificial microRNA interference functions as a potential tumor suppressor in breast cancer. Astrocyte elevated gene-1/MTDH undergoes palmitoylation in normal and abnormal physiology of the cell [13].The microgrooved biomaterial titanium substrata can alter the expression of AEG-1 in human primary cells [14].