ArticleDiscover oncology2022
T cell differentiation protein 2 facilitates cell proliferation by enhancing mTOR-mediated ribosome biogenesis in non-small cell lung cancer.
Article in Discover oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- Integrating Single-Cell, Bulk, and Spatial Transcriptomics Unveils a Novel Ribosome Biogenesis-Related Prognostic Model and DefinesInternational journal of molecular sciences · 2026Article
- Astragalus Polysaccharide Attenuates Breast Cancer Progression by Regulating METTL3-Mediated MAL2 mJournal of microbiology and biotechnology · 2026Article
- Prognostic Value and Related Molecular Mechanisms of miR-5003-3p in Hepatocellular Carcinoma.Canadian journal of gastroenterology & hepatology · 2026Article
- AI-Guided Chemotherapy Optimization in Lung Cancer Using Genomic and Survival Data.Journal of personalized medicine · 2025Article
- Exploring ribosome biogenesis in lung adenocarcinoma to advance prognostic methods and immunotherapy strategies.Journal of translational medicine · 2025Article
- Research advances of MAL family members in tumorigenesis and tumor progression (Review).Molecular medicine reports · 2024Review
- mTOR signalling pathway in stem cell bioactivities and angiogenesis potential.Cell proliferation · 2023Review
- Downregulation of MAL2 inhibits breast cancer progression through regulating β-catenin/c-Myc axis.Cancer cell international · 2023Article
- The MAL Family of Proteins: Normal Function, Expression in Cancer, and Potential Use as Cancer Biomarkers.Cancers · 2023Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Dysregulation of T cell differentiation protein 2 (MAL2) has been observed in multiple cancers, but its exact role in lung cancer is poorly understood. Here we report a role of MAL2 in accelerating cell proliferation in non-small cell lung cancer (NSCLC). MAL2 expression enhances cell proliferation in both cell and nude mouse models. Mechanistically, overexpression of MAL2 results in the hyper-activation of the MAPK/mTOR signaling pathway in NSCLC cells which leads to active ribosome biogenesis. Importantly, pharmacological inhibition of mTOR or MEK lowered the abundance of PCNA, a marker of tumor cell proliferation, and subsequently suppressed ribosome biogenesis, cell growth and xenograft growth in mouse model. MAL2 upregulation in clinical tumors is also linked to worse prognosis. Overall our data reveal that MAL2 is a potential diagnostic biomarker and targeting the MAL2/MAPK/mTOR signaling pathway may improve therapeutic strategy and efficacy for this subset of NSCLC patients.
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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.