ArticleCell death & disease2022
Endothelial cell-specific molecule 1 drives cervical cancer progression.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Transcriptomic Profiling of Canine Testicular Leydig Cell Tumors Uncovers Key Upregulated Gene Pathways.Animals : an open access journal from MDPI · 2026Article
- PFDN5 synergizes with anti-PD1 therapy to promote triple-negative breast cancer cell death through JAK2/STAT3/c-Myc signaling axis.Journal of translational medicine · 2026Article
- PRDM1-driven SLC30A9 overexpression contributes to the malignant phenotype of cervical cancer cells via promoting mitochondrial hyperfunction.Cell death & disease · 2025Article
- Inducible tag-free degradation of endogenous proteins with AlissAID and development of a photoactivable inducer.Communications biology · 2025Article
- Gap junction protein beta 5 interacts with Gαi3 to promote Akt activation and cervical cancer cell growth.Cell death & disease · 2025Article
- IGF2BP3/ESM1/KLF10/BECN1 positive feedback loop: a novel therapeutic target in ovarian cancer via lipid metabolism reprogramming.Cell death & disease · 2025Article
- Single-cell sequencing uncovers a high ESM1-expression endothelial cell subpopulation associated with bladder cancer progression and the immunosuppressive microenvironment.Scientific reports · 2025Article
- Targeting ESM1 via SOX4 promotes the progression of infantile hemangioma through the PI3K/AKT signaling pathway.Precision clinical medicine · 2024Article
- Aloe Emodin Alleviates Radiation-Induced Heart Disease via Blocking P4HB Lactylation and Mitigating Kynurenine Metabolic Disruption.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Screening and identification of susceptibility genes for cervical cancer via bioinformatics analysis and the construction of an mitophagy-related genes diagnostic model.Journal of cancer research and clinical oncology · 2024Article
- The role of ESM1 in the lipids metabolic reprogramming and angiogenesis of lung adenocarcinoma cells.Heliyon · 2024Article
- Methylation of KSHV vCyclin by PRMT5 contributes to cell cycle progression and cell proliferation.PLoS pathogens · 2024Article
- Oncogenic HPV-induced high expression of ESM1 predicts poor prognosis and regulates aerobic glycolysis in cervical cancer.iScience · 2024Article
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- Roles of endothelial cell specific molecule‑1 in tumor angiogenesis (Review).Oncology letters · 2024Review
- Endothelial cell specific molecule 1 promotes epithelial-mesenchymal transition of cervical cancer via the E-box binding homeobox 1.PloS one · 2024Article
- Functional analysis of ESM1 by shRNA-mediated knockdown of its expression in papillary thyroid cancer cells.PloS one · 2024Article
- Elevated expression of endocan in the development of cervical squamous neoplasia of the uterus.Medical molecular morphology · 2023Article
- Targeting ESM1/ VEGFα signaling axis: a promising therapeutic avenue for angiogenesis in cervical squamous cell carcinoma.Journal of Cancer · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression, biological functions and underlying molecular mechanisms of endothelial cell-specific molecule 1 (ESM1) in human cervical cancer remain unclear. Bioinformatics analysis revealed that ESM1 expression was significantly elevated in human cervical cancer tissues, correlating with patients' poor prognosis. Moreover, ESM1 mRNA and protein upregulation was detected in local cervical cancer tissues and various cervical cancer cells. In established and primary cervical cancer cells, ESM1 shRNA or CRISPR/Cas9-induced ESM1 KO hindered cell proliferation, cell cycle progression, in vitro cell migration and invasion, and induced significant apoptosis. Whereas ESM1 overexpression by a lentiviral construct accelerated proliferation and migration of cervical cancer cells. Further bioinformatics studies and RNA sequencing data discovered that ESM1-assocaited differentially expressed genes (DEGs) were enriched in PI3K-Akt and epithelial-mesenchymal transition (EMT) cascades. Indeed, PI3K-Akt cascade and expression of EMT-promoting proteins were decreased after ESM1 silencing in cervical cancer cells, but increased following ESM1 overexpression. Further studies demonstrated that SYT13 (synaptotagmin 13) could be a primary target gene of ESM1. SYT13 silencing potently inhibited ESM1-overexpression-induced PI3K-Akt cascade activation and cervical cancer cell migration/invasion. In vivo, ESM1 knockout hindered SiHa cervical cancer xenograft growth in mice. In ESM1-knockout xenografts tissues, PI3K-Akt inhibition, EMT-promoting proteins downregulation and apoptosis activation were detected. In conclusion, overexpressed ESM1 is important for cervical cancer growth in vitro and in vivo, possibly by promoting PI3K-Akt activation and EMT progression. ESM1 represents as a promising diagnostic marker and potential therapeutic target of cervical cancer.
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