ArticleCancer biology & therapy2020
SEMA4D under the posttranscriptional regulation of HuR and miR-4319 boosts cancer progression in esophageal squamous cell carcinoma.
Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 34 citations in OpenAlex.
- Regulation of Vascular Calcification by M1-Type Macrophage-Derived Semaphorin 4D.International journal of molecular sciences · 2025Article
- Mediating immunosuppressive functions: a new perspective on the complex immunological properties of SEMA4D in the tumor microenvironment.Frontiers in oncology · 2023Article
- MicroRNAs, Tristetraprolin Family Members and HuR: A Complex Interplay Controlling Cancer-Related Processes.Cancers · 2022Review
- SEMA4D/PlexinB1 promotes AML progression via activation of PI3K/Akt signaling.Journal of translational medicine · 2022Article
- Overexpression of miR-651-5p inhibits ultraviolet radiation-induced malignant biological behaviors of sebaceous gland carcinoma cells by targetingAnnals of translational medicine · 2022Article
- Sema4D/Plexin-B1 promotes the progression of osteosarcoma cells by activating Pyk2-PI3K-AKT pathway.Journal of musculoskeletal & neuronal interactions · 2021Article
- A multi-omics study delineates new molecular features and therapeutic targets for esophageal squamous cell carcinoma.Clinical and translational medicine · 2021Article
- Screening and identification of potential biomarkers and therapeutic drugs in melanoma via integrated bioinformatics analysis.Investigational new drugs · 2021Article
- circ_NRIP1 is oncogenic in malignant development of esophageal squamous cell carcinoma (ESCC) via miR-595/SEMA4D axis and PI3K/AKT pathway.Cancer cell international · 2021Article
- SEMA4D Knockdown AttenuatesBioMed research international · 2021Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) is the major type of esophageal carcinoma, one of the main reasons of cancer-caused death. While the therapeutic effect on ESCC patents is still unsatisfactory as a result of tumor aggression, recurrence and metastasis. RNA-binding proteins, microRNAs and specific genes get involved in tumorigenesis and development of tumors in a large proportion. In several reports, SEMA4D is an oncogene and miR-4319 is a tumor suppressor. We discovered the interaction of SEMA4D with HuR and miR-4319, whereas the detailed mechanism in ESCC was yet to be researched. At first, SEMA4D was significantly overexpressed in ESCC cells, and its knockdown repressed cell proliferation and migration as well as accelerated cell apoptosis. And then HuR was proved to stabilize SEMA4D mRNA by binding to its 3'UTR. In addition, miR-4319 targeted and degraded SEMA4D. Taken together, SEMA4D was regulated competitively by HuR and miR-4319. Collectively, HuR and miR-4319 co-regulating SEMA4D affected cell proliferation, apoptosis and migration in ESCC. This research explored the regulatory mechanism on SEMA4D in ESCC and provided optional therapeutic targets for ESCC patients.
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