ArticleOncotarget2016
MTDH is an oncogene in multiple myeloma, which is suppressed by Bortezomib treatment.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- circALPL Sponges miR-127 to Promote Gastric Cancer Progression by Enhancing MTDH Expression.Journal of Cancer · 2021Article
- Retracted Article: Long non-coding RNA PCAT1 facilitates cell growth in multiple myeloma through an MTDH-mediated AKT/β-catenin signaling pathway by sponging miR-363-3p.RSC advances · 2019Article
- The targeting of MTDH by miR‑145‑5p or miR‑145‑3p is associated with prognosis and regulates the growth and metastasis of prostate cancer cells.International journal of oncology · 2019Article
- Metadherin Is a Prognostic Apoptosis Modulator in Mesothelioma Induced via NF-κB-Mediated Signaling.Translational oncology · 2019Article
- Metadherin: A Therapeutic Target in Multiple Cancers.Frontiers in oncology · 2019Review
- Increased AURKA promotes cell proliferation and predicts poor prognosis in bladder cancer.BMC systems biology · 2018Article
- Metadherin regulates actin cytoskeletal remodeling and enhances human gastric cancer metastasis via epithelial-mesenchymal transition.International journal of oncology · 2017Article
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Authors and funding
6 authors.
Funding
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Abstract
Metadherin (MTDH) is identified as an oncogene in multiple cancers including breast cancer, bladder cancer and endometrial cancer. However, the function of MTDH in multiple myeloma (MM) is still unexplored. In this study, we disclose that MTDH is an oncogene in MM. This is characterized by an elevation mRNA level of MTDH and chromosomal gain of MTDH locus in MM cells compared to normal samples. Moreover, MTDH expression significantly increased in MMSET translocation (MS) subgroup, one of the high-risk subgroups in MM, and was significantly correlated with MM patients' poor outcomes in Total Therapy 2 (TT2) cohort. Further knockdown of MTDH expression by shRNA in MM cells induced cell apoptosis, inhibited MM cells growth in vitro and decreased xenograft tumor formation in vivo. Interestingly, opposite to TT2, MM patients with high-MTDH expression showed favorable survival outcomes in the TT3 cohort, while Bortezomib treatment was the major difference between TT2 and TT3 cohort. Furthermore we proved that Bortezomib suppressed pre- and post-transcription levels of MTDH expression of MM cells in vitro and in vivo. Finally, our studies demonstrated that MTDH is a transcriptional gene of MMSET/NFκB /MYC signaling in MM cells, which is inhibited by Bortezomib treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.