ArticleCell reports2014
Sema3C promotes the survival and tumorigenicity of glioma stem cells through Rac1 activation.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
78 citing papers in PubMed, 116 citations in OpenAlex.
- A LINE-1 retrotransposon promotes SEMA3C expression as a cis-regulatory enhancer to sustain breast cancer stem cell survival.Science China. Life sciences · 2026Article
- The SOX4-Semaphorin3C axis promotes esophageal adenocarcinoma progression.Cancer letters · 2025Article
- Elevated nonhomologous end-joining by AATF enables efficient DNA damage repair and therapeutic resistance in glioblastoma.Nature communications · 2025Article
- Construction and validation of a prognostic signature based on microvascular invasion and immune-related genes in hepatocellular carcinoma.Scientific reports · 2024Article
- Article
- Long non-coding RNA lung cancer-associated transcript-1 promotes glioblastoma progression by enhancing Hypoxia-inducible factor 1 alpha activity.Neuro-oncology · 2024Article
- Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression.Signal transduction and targeted therapy · 2024Article
- Hidden secrets of the cancer genome: unlocking the impact of non-coding mutations in gene regulatory elements.Cellular and molecular life sciences : CMLS · 2024Review
- Clinically-observed FOXA1 mutations upregulate SEMA3C through transcriptional derepression in prostate cancer.Scientific reports · 2024Article
- A novel EGFR variant EGFRx maintains glioblastoma stem cells through STAT5.Neuro-oncology · 2024Article
- The semaphorin 3A/neuropilin-1 pathway promotes clonogenic growth of glioblastoma via activation of TGF-β signaling.JCI insight · 2023Article
- Association between circ_0004365 and cisplatin resistance in esophageal squamous cell carcinoma.Oncology letters · 2023Article
- Review
- Extracellular vesicles in the glioblastoma microenvironment: A diagnostic and therapeutic perspective.Molecular aspects of medicine · 2023Review
- Sema3C signaling is an alternative activator of the canonical WNT pathway in glioblastoma.Nature communications · 2023Article
- Plexin-A2 enables the proliferation and the development of tumors from glioblastoma derived cells.Cell death & disease · 2023Article
- Hypoxia-induced HMGB1 promotes glioma stem cells self-renewal and tumorigenicity via RAGE.iScience · 2022Article
- Cross-species single-cell transcriptomic analysis reveals divergence of cell composition and functions in mammalian ileum epithelium.Cell regeneration (London, England) · 2022Article
- Tenascin-C can Serve as an Indicator for the Immunosuppressive Microenvironment of Diffuse Low-Grade Gliomas.Frontiers in immunology · 2022Article
- SEMA3C Supports Pancreatic Cancer Progression by Regulating the Autophagy Process and Tumor Immune Microenvironment.Frontiers in oncology · 2022Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Different cancer cell compartments often communicate through soluble factors to facilitate tumor growth. Glioma stem cells (GSCs) are a subset of tumor cells that resist standard therapy to contribute to disease progression. How GSCs employ a distinct secretory program to communicate with and nurture each other over the nonstem tumor cell (NSTC) population is not well defined. Here, we show that GSCs preferentially secrete Sema3C and coordinately express PlexinA2/D1 receptors to activate Rac1/nuclear factor (NF)-κB signaling in an autocrine/paracrine loop to promote their own survival. Importantly, Sema3C is not expressed in neural progenitor cells (NPCs) or NSTCs. Disruption of Sema3C induced apoptosis of GSCs, but not NPCs or NSTCs, and suppressed tumor growth in orthotopic models of glioblastoma. Introduction of activated Rac1 rescued the Sema3C knockdown phenotype in vivo. Our study supports the targeting of Sema3C to break this GSC-specific autocrine/paracrine loop in order to improve glioblastoma treatment, potentially with a high therapeutic index.
Indexed as
Identifiers
What OpenQuestion holds
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.