ArticleFrontiers in molecular biosciences2019
Alternative Splicing of MXD3 and Its Regulation of MXD3 Levels in Glioblastoma.
Article in Frontiers in molecular biosciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Assessment of MXD3 Expression as a Predictor of Survival in Lung Squamous Cell Carcinoma.International journal of genomics · 2025Article
- Article
- The role of alternative pre-mRNA splicing in cancer progression.Cancer cell international · 2023Review
- A Novel Splice Variant ofCancers · 2022Article
- Review
- MXD3 Promotes Obesity and the Androgen Receptor Signaling Pathway in Gender-Disparity Hepatocarcinogenesis.Cells · 2021Article
- Overexpression of MAX dimerization protein 3 (MXD3) predicts poor prognosis in clear cell renal cell carcinoma.Translational andrology and urology · 2021Article
- Common variation of the NSD1 gene is associated with susceptibility to Hirschsprung's disease in Chinese Han population.Pediatric research · 2021Article
- MXD3 as an onco-immunological biomarker encompassing the tumor microenvironment, disease staging, prognoses, and therapeutic responses in multiple cancer types.Computational and structural biotechnology journal · 2021Article
- MXD3 as an Immunological and Prognostic Factor From Pancancer Analysis.Frontiers in molecular biosciences · 2021Article
- Expression profiles of the MXD3 gene and association of sequence variants with growth traits in Xianan and Qinchuan cattle.Veterinary medicine and science · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factor MXD3 is an atypical member of the MYC/MAX/MXD transcriptional network and has been previously shown to be an important regulator of cell proliferation. MXD3 has been shown to be overexpressed and to be required for medulloblastoma and acute lymphoblastic leukemia cell proliferation. In this study we leveraged datasets from The Cancer Genome Atlas to examine MXD3 across several cancers. We find that MXD3 transcripts are significantly overexpressed in ~72% of the available datasets. The gene itself is not frequently altered, while the promoter appears to be hypomethylated. We examine the possibility that aberrant regulation of the MXD3 message is the cause of abnormal MXD3 expression across cancers. Specifically, we looked at MXD3 alternative splicing in glioblastoma multiforme (GBM) and find notable functional differences between the splice variants. The 3'UTR confers differential message stability. Furthermore, the different coding sequences lead to different protein stabilities and localizations. Altogether, these data extend our knowledge of MXD3 in the context of human cancers while characterizing a previously unstudied splice variant of MXD3.
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Registered trials
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.