ArticleCell death and differentiation2018
Sema4C/PlexinB2 signaling controls breast cancer cell growth, hormonal dependence and tumorigenic potential.
Article in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 49 papers.
What it found
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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.
Diagnosis Value of SEMA4C in Breast Cancer
SEMA4C as a Relapse Biomarker in Breast Cancer
Who cites it
49 citing papers in PubMed, 83 citations in OpenAlex.
- Construction of a lncRNA-mediated ceRNA network and a genomic-clinicopathologic nomogram to predict survival for breast cancer patients.Cancer biomarkers : section A of Disease markers · 2023Trial
- SEMA4F Regulates the Malignant Phenotype of Hepatocellular Carcinoma Cells Through the PI3K-Akt Pathway.Journal of hepatocellular carcinoma · 2026Article
- Context-Dependent Dual Roles of the Plexin-B Family in Cancer Progression: Mechanisms and Therapeutic Implications.Cancer management and research · 2026Review
- Computational ranking identifies Plexin-B2 in circulating tumor cell clustering with monocytes in breast cancer metastasis.Nature communications · 2025Article
- Boric Acid Induces Oxidative Damage and Apoptosis Through SEMA3A/PLXNA1/NRP1 Signalling Pathway in U251 Glioblastoma Cell.Journal of cellular and molecular medicine · 2025Article
- Inhibiting glycolysis facilitated checkpoint blockade therapy for triple-negative breast cancer.Discover oncology · 2025Article
- Review
- PRMT5 Maintains Tumor Stem Cells to Promote Pediatric High-Grade Glioma Tumorigenesis.Molecular cancer research : MCR · 2025Article
- Robust collection and processing for label-free single voxel proteomics.Nature communications · 2025Article
- Exploring the impact of circRNAs on cancer glycolysis: Insights into tumor progression and therapeutic strategies.Non-coding RNA research · 2024Review
- Involvement of neuronal factors in tumor angiogenesis and the shaping of the cancer microenvironment.Frontiers in immunology · 2024Review
- Large-scale analysis of cell-cell communication reveals angiogenin-dependent tumor progression in clear cell renal cell carcinoma.iScience · 2023Article
- DNA damage repair molecular subtype derived immune signature applicable for the prognosis and immunotherapy response prediction in colon cancer.Translational cancer research · 2023Article
- Semaphorins and Their Roles in Breast Cancer: Implications for Therapy Resistance.International journal of molecular sciences · 2023Review
- Review
- Whole exome sequencing in unexplained recurrent miscarriage families identified novel pathogenic genetic causes of euploid miscarriage.Human reproduction (Oxford, England) · 2023Article
- From Biology to Diagnosis and Treatment: The Ariadne's Thread in Cancer of Unknown Primary.International journal of molecular sciences · 2023Review
- Mutated axon guidance gene PLXNB2 sustains growth and invasiveness of stem cells isolated from cancers of unknown primary.EMBO molecular medicine · 2023Article
- Targeting ARHGEF12 promotes neuroblastoma differentiation, MYCN degradation, and reduces tumorigenicity.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Plexin-A2 enables the proliferation and the development of tumors from glioblastoma derived cells.Cell death & disease · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Semaphorin 4C (Sema4C) expression in human breast cancers correlates with poor disease outcome. Surprisingly, upon knock-down of Sema4C or its receptor PlexinB2 in diverse mammary carcinoma cells (but not their normal counterparts), we observed dramatic growth inhibition associated with impairment of G2/M phase transition, cytokinesis defects and the onset of cell senescence. Mechanistically, we demonstrated a Sema4C/PlexinB2/LARG-dependent signaling cascade that is required to maintain critical RhoA-GTP levels in cancer cells. Interestingly, we also found that Sema4C upregulation in luminal-type breast cancer cells drives a dramatic phenotypic change, with disassembly of polarity complexes, mitotic spindle misorientation, cell-cell dissociation and increased migration and invasiveness. We found that this signaling cascade is dependent on the PlexinB2 effectors ErbB2 and RhoA-dependent kinases. Moreover, Sema4C-overexpressing luminal breast cancer cells upregulated the transcription factors Snail, Slug and SOX-2, and formed estrogen-independent metastatic tumors in mice. In sum, our data indicate that Sema4C/PlexinB2 signaling is essential for the growth of breast carcinoma cells, featuring a novel potential therapeutic target. In addition, elevated Sema4C expression enables indolent luminal-type tumors to become resistant to estrogen deprivation, invasive and metastatic in vivo, which could account for its association with a subset of human breast cancers with poor prognosis.
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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.