ArticleOncotarget2017
Tumor p38MAPK signaling enhances breast carcinoma vascularization and growth by promoting expression and deposition of pro-tumorigenic factors.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Immune-related LncRNA signatures define tumor microenvironment subtypes and predict immunotherapy response in NSCLC.Discover oncology · 2026Article
- Cancer-associated fibroblast miR-148a-5p/CALD1/collagen VI pathway promotes proliferation in Helicobacter pylori-positive gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- p38 blockade reverses the immune suppressive tumor microenvironment in metastatic breast cancer.Research square · 2025Article
- TGFβ1-TNFα-regulated secretion of neutrophil chemokines is independent of epithelial-mesenchymal transition in breast tumor cells.Molecular biology of the cell · 2025Article
- BRAT1 - a new therapeutic target for glioblastoma.Cellular and molecular life sciences : CMLS · 2025Article
- Effects of Platycodon grandiflorus on doxorubicin resistance and epithelial-mesenchymal transition of breast cancer cells via the p38 mitogen-activated protein kinase pathway.Journal of molecular histology · 2024Article
- PXD101 inhibits malignant progression and radioresistance of glioblastoma by upregulating GADD45A.Journal of translational medicine · 2024Article
- Unveiling the Nexus: Cellular Metabolomics Unravels the Impact of Estrogen on Nicotinamide Metabolism in Mitigating Rheumatoid Arthritis Pathogenesis.Metabolites · 2024Article
- Echinatin inhibits tumor growth and synergizes with chemotherapeutic agents against human bladder cancer cells by activating p38 and suppressing Wnt/β-catenin pathways.Genes & diseases · 2024Article
- Article
- Association of Promoter Methylation Patterns with Expression of MAPK14 in Tissue of Papillary Thyroid Cancer Patients.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Anastasis confers ovarian cancer cells increased malignancy through elevated p38 MAPK activation.Cell death and differentiation · 2023Article
- Stress signaler p38 mitogen-activated kinase activation: a cause for concern?Clinical science (London, England : 1979) · 2022Article
- New Insights into SARS-CoV-2 and Cancer Cross-Talk: Does a Novel Oncogenesis Driver Emerge?Vaccines · 2022Review
- Mapk14 is a Prognostic Biomarker and Correlates with the Clinicopathological Features and Immune Infiltration of Colorectal Cancer.Frontiers in cell and developmental biology · 2022Article
- Unraveling the molecular mechanisms between inflammation and tumor angiogenesis.American journal of cancer research · 2021Review
- Novel Pathways for Targeting Tumor Angiogenesis in Metastatic Breast Cancer.Frontiers in oncology · 2021Review
- Blockade of p38 kinase impedes the mobilization of protumorigenic myeloid populations to impact breast cancer metastasis.International journal of cancer · 2020Article
- Elucidating the molecular signaling pathways of WAVE3.Annals of translational medicine · 2020Review
- 90 YEARS OF PROGESTERONE: Steroid receptors as MAPK signaling sensors in breast cancer: let the fates decide.Journal of molecular endocrinology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
The breast carcinoma microenvironment strikingly influences cancer progression and response to therapy. Various cell types in the carcinoma microenvironment show significant activity of p38 mitogen-activated protein kinase (MAPK), although the role of p38MAPK in breast cancer progression is still poorly understood. The present study examined the contribution of tumor p38MAPK to breast carcinoma microenvironment and metastatic capacity. Inactivation of p38MAPK signaling in metastatic breast carcinoma cells was achieved by forced expression of the kinase-inactive mutant of p38/MAPK14 (a dominant-negative p38, dn-p38). Disruption of tumor p38MAPK signaling reduced growth and metastases of breast carcinoma xenografts. Importantly, dn-p38 markedly decreased tumor blood-vessel density and lumen sizes. Mechanistic studies revealed that p38 controls expression of pro-angiogenic extracellular factors such as matrix protein Fibronectin and cytokines VEGFA, IL8, and HBEGF. Tumor-associated fibroblasts enhanced tumor growth and vasculature as well as increased expression of the pro-angiogenic factors. These effects were blunted by dn-p38. Metadata analysis showed elevated expression of p38 target genes in breast cancers and this was an unfavorable marker of disease recurrence and poor-outcome. Thus, our study demonstrates that tumor p38MAPK signaling promotes breast carcinoma growth, invasive and metastatic capacities. Importantly, p38 enhances carcinoma vascularization by facilitating expression and deposition of pro-angiogenic factors. These results argue that p38MAPK is a valuable target for anticancer therapy affecting tumor vasculature. Anti-p38 drugs may provide new therapeutic strategies against breast cancer, including metastatic disease.
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