ArticlePloS one2015
The Phosphoinositide 3-Kinase p110α Isoform Regulates Leukemia Inhibitory Factor Receptor Expression via c-Myc and miR-125b to Promote Cell Proliferation in Medulloblastoma.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
- Targeting LIF/LIFR signaling in cancer.Genes & diseases · 2022Review
- The Pleiotropic role, functions and targeted therapies of LIF/LIFR axis in cancer: Old spectacles with new insights.Biochimica et biophysica acta. Reviews on cancer · 2022Review
- Wnt and PI3K/Akt/mTOR Survival Pathways as Therapeutic Targets in Glioblastoma.International journal of molecular sciences · 2022Review
- Immunosuppression in Medulloblastoma: Insights into Cancer Immunity and Immunotherapy.Current treatment options in oncology · 2021Review
- Epigenetic-Based Therapy-A Prospective Chance for Medulloblastoma Patients' Recovery.International journal of molecular sciences · 2021Review
- Tumor Growth in the High Frequency Medulloblastoma Mouse Model Ptch1Frontiers in oncology · 2021Article
- Emerging Perspectives on Leukemia Inhibitory Factor and its Receptor in Cancer.Frontiers in oncology · 2021Review
- The Emerging Field of Noncoding RNAs and Their Importance in Pediatric Diseases.The Journal of pediatrics · 2020Article
- The Non-coding Side of Medulloblastoma.Frontiers in cell and developmental biology · 2020Review
- Pharmacological mTOR targeting enhances the antineoplastic effects of selective PI3Kα inhibition in medulloblastoma.Scientific reports · 2019Article
- The Roles of miRNAs in Medulloblastoma: A Systematic Review.Journal of cancer prevention · 2019Review
- c-Myc activation promotes cofilin-mediated F-actin cytoskeleton remodeling and telomere homeostasis as a response to oxidant-based DNA damage in medulloblastoma cells.Redox biology · 2019Article
- Potent Antineoplastic Effects of Combined PI3Kα-MNK Inhibition in Medulloblastoma.Molecular cancer research : MCR · 2019Article
- STAT3 activation confers trastuzumab-emtansine (T-DM1) resistance in HER2-positive breast cancer.Cancer science · 2018Article
- Leptin Involvement in Primary Brain and Pituitary Tumors: Therapeutic Potential, Prognostic Value, and Proposed Diagnostic Application.Hormones & cancer · 2018Review
- miR-125b suppresses the proliferation of hepatocellular carcinoma cells by targeting Sirtuin7.International journal of clinical and experimental medicine · 2015Article
- Thrombospondin-1 mimetics are promising novel therapeutics for MYC-associated medulloblastoma.Neuro-oncology advancesArticle
- The therapeutic and diagnostic potential of regulatory noncoding RNAs in medulloblastoma.Neuro-oncology advancesReview
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Medulloblastoma (MB) is the most common malignant brain tumor in childhood and represents the main cause of cancer-related death in this age group. The phosphoinositide 3-kinase (PI3K) pathway has been shown to play an important role in the regulation of medulloblastoma cell survival and proliferation, but the molecular mechanisms and downstream effectors underlying PI3K signaling still remain elusive. The impact of RNA interference (RNAi)-mediated silencing of PI3K isoforms p110α and p110δ on global gene expression was investigated by DNA microarray analysis in medulloblastoma cell lines. A subset of genes with selectively altered expression upon p110α silencing in comparison to silencing of the closely related p110δ isoform was revealed. Among these genes, the leukemia inhibitory factor receptor α (LIFR α) was validated as a novel p110α target in medulloblastoma. A network involving c-Myc and miR-125b was shown to be involved in the control of LIFRα expression downstream of p110α. Targeting the LIFRα by RNAi, or by using neutralizing reagents impaired medulloblastoma cell proliferation in vitro and induced a tumor volume reduction in vivo. An analysis of primary tumors revealed that LIFRα and p110α expression were elevated in the sonic hedgehog (SHH) subgroup of medulloblastoma, indicating its clinical relevance. Together, these data reveal a novel molecular signaling network, in which PI3K isoform p110α controls the expression of LIFRα via c-Myc and miR-125b to promote MB cell proliferation.
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