ArticleJournal of translational medicine2022
Membrane progesterone receptor α (mPRα) enhances hypoxia-induced vascular endothelial growth factor secretion and angiogenesis in lung adenocarcinoma through STAT3 signaling.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- Dual regulation of autophagy: paradoxical effects on tumor angiogenesis.Frontiers in cell and developmental biology · 2026Review
- Lactylation-driven PDLIM1/PDAP1 axis remodels the inflammatory landscape of acute lung injury: mechanistic insights and precision intervention.Frontiers in immunology · 2026Article
- LINC00313 functions as an oncogenic propellant and immunosuppressive marker in lung adenocarcinoma.Future science OA · 2025Article
- The Clinical Implications of Progesterone in Preeclampsia.Biomolecules · 2025Review
- Keratin 80 as a diagnostic biomarker with limited prognostic value in non-small cell lung cancer.Scientific reports · 2025Article
- The Suppression of Signal Transducer and Activator of Transcription-3 in A549 human Lung Carcinoma Cells Induced by Marine SpongeJournal of experimental pharmacology · 2025Article
- Regulation of VEGF-A expression and VEGF-A-targeted therapy in malignant tumors.Journal of cancer research and clinical oncology · 2024Review
- Expression of lncRNA LINC00943 in lung squamous cell carcinoma and its relationship with tumor progression.Journal of cardiothoracic surgery · 2024Article
- Angiogenesis modulated by CD93 and its natural ligands IGFBP7 and MMRN2: a new target to facilitate solid tumor therapy by vasculature normalization.Cancer cell international · 2023Review
- Complement factor H inhibits endothelial cell migration through suppression of STAT3 signaling.Experimental and therapeutic medicine · 2023Article
- New Perspectives on Sex Steroid Hormones Signaling in Cancer-Associated Fibroblasts of Non-Small Cell Lung Cancer.Cancers · 2023Review
- CmPn/CmP Signaling Networks in the Maintenance of the Blood Vessel Barrier.Journal of personalized medicine · 2023Review
- Role of gonadally synthesized steroid hormones in the colorectal cancer microenvironment.Frontiers in oncology · 2023Review
- The Role of MRE11 in the IL-6/STAT3 Pathway of Lung Cancer Cells.Current issues in molecular biology · 2022Article
- The Interaction Between Autophagy and JAK/STAT3 Signaling Pathway in Tumors.Frontiers in genetics · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Lung cancer remains a huge challenge to public health because of its high incidence and mortality, and lung adenocarcinoma (LUAD) is the main subtype of lung cancer. Hypoxia-induced vascular endothelial growth factor (VEGF) release and angiogenesis have been regarded as critical events in LUAD carcinogenesis. In the present study, membrane progesterone receptor α (mPRα) is deregulated within LUAD tissue samples; increased mPRα contributes to a higher microvessel density (MVD) in LUAD tissues. mPRα knockdown in A549 and PC-9 cells significantly inhibited STAT3 phosphorylation, as well as HIF1α and VEGF protein levels, decreasing cancer cell migration and invasion. The in vivo xenograft model further confirmed that mPRα enhanced the aggressiveness of LUAD cells. Furthermore, mPRα knockdown significantly inhibited hypoxia-induced upregulation in HIF1α and VEGF levels, as well as LUAD cell migration and invasion. Under the hypoxic condition, conditioned medium (CM) derived from mPRα knockdown A549 cells, namely si-mPRα-CM, significantly inhibited HUVEC migration and tube formation and decreased VEGF level in the culture medium. In contrast, CM derived from mPRα-overexpressing A549 cells, namely mPRα-CM, further enhanced HUVEC migration and tube formation and increased VEGF level under hypoxia, which was partially reversed by STAT3 inhibitor Stattic. In conclusion, in LUAD cells, highly expressed mPRα enhances the activation of cAMP/JAK/STAT3 signaling and increases HIF1α-induced VEGF secretion into the tumor microenvironment, promoting HUVEC migration and tube formation under hypoxia.
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