ArticleMolecular carcinogenesis2019
NRP-1 interacts with GIPC1 and SYX to activate p38 MAPK signaling and cancer stem cell survival.
Article in Molecular carcinogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Neuropilins in Multiple Sclerosis: Dual Roles of NRP-1 in Neuroinflammation and Neuroprotection.Neuromolecular medicine · 2026Review
- The Role of the TG2-GPR56 Complex in Cutaneous Squamous Cell Carcinoma (CSCC) Aggression and Therapeutic Resistance.International journal of molecular sciences · 2026Review
- GIPC1 Restrains the Progression and Chemoresistance of Colorectal Cancer by Regulating TTC7B/mTOR/NF-κB Axis.International journal of biological sciences · 2026Article
- Comparing self-reported race and genetic ancestry for identifying potential differentially methylated sites in endometrial cancer: insights from African ancestry proportions using machine learning models.Molecular oncology · 2025Article
- Implications of Raftlin in different diseases: from molecular biology to diagnostic value.Biomarkers in medicine · 2025Review
- NRP1 knockdown inhibits the invasion and migration of rhabdoid tumor of the kidney cells.Pediatric surgery international · 2024Article
- Preclinical evaluation ofEuropean journal of nuclear medicine and molecular imaging · 2024Article
- Revealing neuropilin expression patterns in pancreatic cancer: From single‑cell to therapeutic opportunities (Review).Oncology letters · 2024Review
- The transglutaminase 2 cancer cell survival factor maintains mTOR activity to drive an aggressive cancer phenotype.Molecular carcinogenesis · 2023Article
- Neuropilin (NRPs) Related Pathological Conditions and Their Modulators.International journal of molecular sciences · 2022Review
- Transglutaminase 2 enhances hepatocyte growth factor signaling to drive the mesothelioma cancer cell phenotype.Molecular carcinogenesis · 2022Article
- Transglutaminase 2 Maintains Hepatocyte Growth Factor Signaling to Enhance the Cancer Cell Phenotype.Molecular cancer research : MCR · 2021Article
- VGLL4 inhibits YAP1/TEAD signaling to suppress the epidermal squamous cell carcinoma cancer phenotype.Molecular carcinogenesis · 2021Article
- Harnessing the polyamine transport system to treat BRAF inhibitor-resistant melanoma.Cancer biology & therapy · 2021Article
- Role of NRP1 in Bladder Cancer Pathogenesis and Progression.Frontiers in oncology · 2021Article
- 90 YEARS OF PROGESTERONE: Steroid receptors as MAPK signaling sensors in breast cancer: let the fates decide.Journal of molecular endocrinology · 2020Review
- PLEKHG5 is a novel prognostic biomarker in glioma patients.International journal of clinical oncology · 2019Article
- Transglutaminase 2 takes center stage as a cancer cell survival factor and therapy target.Molecular carcinogenesis · 2019Article
- Targeting Neuropilin-1 for Cancer Pain Treatment: A Trial With Potential for Clinical Translation.Cancer control : journal of the Moffitt Cancer CenterReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Epidermal cancer stem cells (ECS cells) comprise a limited population of cells that form aggressive, rapidly growing, and highly vascularized tumors. VEGF-A/NRP-1 signaling is a key driver of the ECS cell phenotype and aggressive tumor formation. However, relatively less is known regarding the downstream events following VEGF-A/NRP-1 interaction. In the present study, we show that VEGF-A/NRP-1, GIPC1, and Syx interact to increase RhoA-dependent p38 MAPK activity to enhance ECS cell spheroid formation, invasion, migration, and angiogenic potential. Inhibition or knockdown of NRP-1, GIPC1 or Syx attenuates RhoA and p38 activity to reduce the ECS cell phenotype, and NRP-1 knockout, or pharmacologic inhibition of VEGF-A/NRP-1 interaction or RhoA activity, reduces p38 MAPK activity and tumor growth. Moreover, expression of wild-type or constitutively-active RhoA, or p38, in NRP1-knockout cells, restores p38 activity and the ECS cell phenotype. These findings suggest that NRP-1 forms a complex with GIPC1 and Syx to activate RhoA/ROCK-dependent p38 activity to enhance the ECS cell phenotype and tumor formation.
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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.