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Last update 08 May 2025

MTDH

Last update 08 May 2025

Basic Info

Synonyms

3D3, 3D3/LYRIC, AEG-1

+ [8]

Introduction

Down-regulates SLC1A2/EAAT2 promoter activity when expressed ectopically. Activates the nuclear factor kappa-B (NF-kappa-B) transcription factor. 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 effect on bone and brain metastasis, possibly by enhancing the seeding of tumor cells to the target organ endothelium. Induces chemoresistance.

Drugs associated with MTDH

C26-A6

Target

MTDH

Mechanism

MTDH inhibitors

Active Org.

Virginia Commonwealth University

Originator Org.

Virginia Commonwealth University

Active Indication

Hepatocellular Carcinoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

MTDH/SND1 inhibitors(China Pharmaceutical University)

Target

MTDH x SND1

Mechanism

MTDH inhibitors [+1]

Active Org.

China Pharmaceutical University

Originator Org.

China Pharmaceutical University

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN115066247

Patent Mining

Target

MTDH

Mechanism-

Active Org.

Secarna Pharmaceuticals Gmbh & Co.

Originator Org.

Secarna Pharmaceuticals Gmbh & Co.

Active Indication

Endocrinology and Metabolic Disease [+4]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MTDH

100 Translational Medicine associated with MTDH

0 Patents (Medical) associated with MTDH

767

Literatures (Medical) associated with MTDH

31 Dec 2025·Annals of Medicine

MicroRNA-122 overexpression suppresses the colon cancer cell proliferation by downregulating the astrocyte elevated gene-1/metadherin oncoprotein

Article

Author: Banerjee, Antara ; Malayaperumal, Sarubala ; Zhang, Hong ; NR, Rajesh Kanna ; Pathak, Surajit ; Sun, Xiao-Feng ; Mohammed Rafi, Shabana Thabassum ; Jothimani, Ganesan ; Ramachandran, Ilangovan ; Sriramulu, Sushmitha

BACKGROUNDMicroRNAs (miRNAs) are small non-coding RNAs that regulate essential cellular functions, such as cell adhesion, proliferation, migration, invasion, and programmed cell death, and therefore, alterations in miRNAs can contribute to carcinogenesis. Previous studies have shown that miRNA-122 is abundant in the liver and regulates cell proliferation, migration, and apoptosis. However, the expression pattern and mechanism of actions of miR-122 remain primarily unknown in colon cancer.METHODSIn this study, we analyzed The Cancer Genome Atlas Colon Adenocarcinoma (TCGA-COAD) database to assess the clinical significance of astrocyte elevated gene-1 (AEG-1)/metadherin (MTDH) and miR-122 in colon cancer. MiR-122 overexpression studies were performed in HCT116, SW480, and SW620 cell lines. Dual-luciferase assay was carried out to confirm the interaction between AEG-1 and miR-122. In vivo-JetPEI-transfection reagent was used for in-vivo transient transfection of miR-122 in the AOM/DSS-induced colon tumor mouse model.RESULTSOur results demonstrate that miR-122 was downregulated in colon cancer cells, and it influences the expressions of apoptotic factors and inflammatory cytokines. MiR-122 overexpression in HCT116, SW480, and SW620 cells showed upregulation of Caspase 3, Caspase 9, and BAX and decreased expression of BCL2, which are pro-apoptotic and anti-apoptotic members that maintain a ratio between cellular survival and cell death. In vivo transient transfection of miR-122 mimic in AOM/DSS induced colon tumor mouse model showed less inflammation and disease activity. The TCGA-COAD data indicated that AEG-1 expression was higher in patients with low expression of miR-122 and lower AEG-1 expression in patients with higher expression miR-122.CONCLUSIONOur findings highlight the key role of miR-122 in the high grade of colonic inflammation, and possibly in colon cancer, and the use of miR-122 mimic might be a therapeutic option.

01 Jul 2025·Brain, Behavior, and Immunity

Astrocyte elevated gene-1 (AEG-1) in myeloid cells is a key driver for the development of chemotherapy-induced peripheral neuropathy

Article

Author: Sarkar, Devanand ; Bryan, Tayla ; Damaj, M Imad ; Herz, Sara M ; Mckiver, Bryan D ; Salem, Aliasger K ; Poklis, Justin L ; Bigbee, John W ; Windle, Jolene J ; Patel, Shivani ; Mann, Jared

Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting side effect of chemotherapy treatment, often resulting in the discontinuation of treatment. Paclitaxel activates peripheral macrophages, generating a neuroinflammatory response that contributes to CIPN development and maintenance. Astrocyte Elevated Gene-1 (AEG-1), also known as Metadherin or LYRIC, is a multifunctional protein that modulates macrophage activity and regulates inflammation through direct interaction with NF-κB, a transcriptional regulator of proinflammatory cytokine/chemokine (PIC) expression. We aimed to determine whether AEG-1 contributes to the development and maintenance of CIPN pathologies by using both global (AEG-1 KO) and myelocyte-specific knockout (AEG-1ΔMAC) transgenic mouse strains in an animal model of CIPN that replicates specific human clinical phenotypes. We hypothesized that inhibition of AEG1 expression in myeloid cells, such as monocytes and macrophages, would prevent the development and maintenance of CIPN. Our results showed that global AEG-1 deletion prevented the development of CIPN pathologies induced by PAC, as well as oxaliplatin (OHP). PAC treatment was found to increase AEG-1 and PIC expression in the DRGs of WT mice and in peritoneal macrophages isolated from C57BL/6J mice. However, in the absence of AEG-1 expression, PAC-induced neuroinflammation was completely halted in the DRGs of AEG-1 KO mice. This preventative phenotype and PIC expression profile was mirrored in AEG-1ΔMAC mice, which also displayed reduced NF-κB protein levels and F4/80+ macrophages trafficked to the lumbar DRGs following PAC treatment. In summary, our results are the first to demonstrate the biological role AEG-1, particularly in myeloid cells, in development of CIPN.

01 Jun 2025·European Journal of Pharmacology

Sinomenine ameliorates vascular calcification by inhibiting pyroptosis-related molecules and AEG-1 in chronic kidney disease

Article

Author: Tang, Zixu ; Fu, Haojun ; Zhong, Shuzhu ; Xia, Yuan ; Peng, Zhong ; Yu, Fengyi ; Long, Wei ; Liao, Zihao ; Zhao, Song ; He, Zhangxiu ; Gao, Ning

BACKGROUNDSVascular calcification (VC) is an important factor for mortality in chronic kidney disease (CKD). Sinomenine can suppress atherosclerosis. However, its role in CKD-associated-vascular calcification and mechanisms remain unclear.METHODSSprague-Dawley rats that were fed with high-phosphorus diet and adenine suspension were used to construct the calcification model in CKD. Calcification from rats or cells were analyzed using micro-CT and alizarin red staining. Levels of NLRP-3, Caspase-1, GSDMD and AEG-1 were measured by qPCR, western blotting, and immunohistochemistry. Transfection experiment was used in function study.RESULTSCKD rats fed with high-phosphorus diet and adenine suspension increased aortic calcification over time. Micro-CT images revealed the distribution and severity of the calcification, and these lesions were significantly decreased in the Sinomenine (SIN) group. This is similar to the results obtained for the AR staining of translucent samples. Additionally, aortas from CKD rats that were treated with 30 mg/kg/d SIN showed a down-regulation of NLRP3, Caspase-1, GSDMD and AEG-1 expression compared with aortas from CKD rats. Sinomenine exhibited similar inhibitory effects on NLRP3 and Caspase-1 as VX-765 in the aortas of uremic rats and calcified VSMCs. Moreover, VSMC transfected with pc-AEG-1 accelerated the VSMC calcification while transfection with si-AEG-1 ameliorated the calcification. Importantly, sinomenine abolished the VSMC calcification induced by AEG-1 overexpression under the uremia condition.CONCLUSIONSOur findings indicated that sinomenine could ameliorate vascular calcification in CKD rats and inhibit hyperphosphatemia-induced calcifying VSMCs via inhibiting pyroptosis-related molecules and AEG-1. Sinomenine might serve as an effective therapeutic agent for CKD-associated vascular calcification.

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MTDH

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