ArticleJournal of experimental & clinical cancer research : CR2020
SM22α
Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Macrophage membrane-functionalized biomimetic Yiqi Huoxue formula nanoparticles improve atherosclerosis by regulating smooth muscle cell phenotypic transition via the KLF4/NF-κB pathway.Chinese medicine · 2026Article
- EphB4/EphrinB2 signaling regulates pericyte-like function of DPSCs in angiogenesis via transcriptional factor SRF.Stem cell research & therapy · 2026Article
- Natural medicines target tumor vascular microenvironment to inhibit tumor.Genes & diseases · 2025Review
- Targeting Regulatory Noncoding RNAs in Human Cancer: The State of the Art in Clinical Trials.Pharmaceutics · 2025Review
- Article
- CAFs vs. TECs: when blood feuds fuel cancer progression, dissemination and therapeutic resistance.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Non-Coding RNAs of Mitochondrial Origin: Roles in Cell Division and Implications in Cancer.International journal of molecular sciences · 2024Review
- Neural regulation of mesenchymal stem cells in craniofacial bone: development, homeostasis and repair.Frontiers in physiology · 2024Review
- Mechanical regulation of the early stages of angiogenesis.Journal of the Royal Society, Interface · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMalformation of blood vessels represents a hallmark of cancers, but the role and regulation of vascular mural cells (vMCs), including vascular smooth muscle cells (vSMCs) and pericytes, in tumors has not been fully understood. SM22α has been identified as a marker of vSMCs. This study aims at elucidating the function and regulation of SM22α
methodsGene-modified mice with a SM22α-CreER
resultsSM22-MCs are essential for stabilizing tumor vasculature. Notch signaling was downregulated in tumor-derived SM22-MCs and vSMCs-DA treated with cancer cell-derived conditioned medium. Notch activation in SM22-MCs normalized tumor vasculature and repressed tumor growth. On the other hand, Notch disruption aggravated abnormal tumor vasculature and promoted growth and metastasis. Gene expression profiling of vSMCs-DA showed that Notch activation enhances their contractile phenotype and suppresses their secretory phenotype, further attenuating the invasion and proliferation of tumor cells. In contrast, Notch blockade in vSMCs-DA mitigated their contractile phenotype while strengthened the secretory phenotype.
conclusionSM22-MCs facilitate vessel stability in tumors, and they gain a secretory phenotype and promote tumor malignancy in the absence of Notch signaling.
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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.