ArticleCancer immunology, immunotherapy : CII2013
A knockdown of Maml1 that results in melanoma cell senescence promotes an innate and adaptive immune response.
Article in Cancer immunology, immunotherapy : CII, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Role of Ferredoxin 1Cancer pathogenesis and therapy · 2026Review
- Illuminating the immunological landscape: mitochondrial gene defects in pancreatic cancer through a multiomics lens.Frontiers in immunology · 2024Review
- Circadian clock protein CRY1 prevents paclitaxel‑induced senescence of bladder cancer cells by promoting p53 degradation.Oncology reports · 2021Article
- Cancer Cell enters reversible quiescence through Intracellular Acidification to resist Paclitaxel Cytotoxicity.International journal of medical sciences · 2020Article
- Negative Regulatory Loop between Microphthalmia-Associated Transcription Factor (MITF) and Notch Signaling.International journal of molecular sciences · 2019Article
- Notch1 signaling in melanoma cells promoted tumor-induced immunosuppression via upregulation of TGF-β1.Journal of experimental & clinical cancer research : CR · 2018Article
- Cancer Cells Exploit Notch Signaling to Redefine a Supportive Cytokine Milieu.Frontiers in immunology · 2018Review
- Epigenetic alteration to activate Bmp2-Smad signaling in Raf-induced senescence.World journal of biological chemistry · 2016Article
- Shp2 signaling suppresses senescence in PyMT-induced mammary gland cancer in mice.The EMBO journal · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maml1 is emerging as a coactivator of many signaling pathways, including the Notch and Wnt pathways. Targeting Maml1 in melanoma cells efficiently knocks down the downstream transcriptional repressors Hey1 and Hes1, resulting in melanoma cell senescence, cellular differentiation, and increased melanin production. Significantly, higher IFNβ and chemokine gene transcripts have been observed, together with increased STAT1 and decreased STAT3 and NF-κB signaling activities. Although decreased cell proliferation contributes to slower tumor growth in vivo, the depletion of NK and CD8(+) T cells in an shMaml1-B16 tumor carrier mouse leads to more rapid tumor growth than that observed in control shC002-B16 tumors. This result demonstrates that the knockdown of Maml1 transcription and function contributes to increased immune surveillance. The knockdown of Maml1 transcription in the human melanoma cell line M537 also results in senescence, IFNβ upregulation, increased chemokine gene expression, and greater NK and CD8(+) T cell migration in a transwell system. This study demonstrated that targeting Maml1-induced tumor cell senescence and differentiation may alter the tumor microenvironment and cytokine and chemokine profiles and may also promote innate and adaptive immune cell infiltration and function.
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Registered trials
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