International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.
International Journal of Oncology is an international journal devoted to oncology research and cancer treatment.
Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.
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Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology.
International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis.
Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology.
Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition.
Publishes open-access research on using epigenetics to advance understanding and treatment of human disease.
An International Open Access Journal Devoted to General Medicine.
miRNA‑29a inhibits the proliferation of HUVECs by regulating the ITGB1/β‑catenin/c‑Myc pathway
Infantile hemangioma (IH) is a type of benign vascular tumor observed in younger patients. Previously, 216 differentially expressed microRNAs (miRs/miRNAs) associated with IH have been identified. In addition, common hub genes and miRNAs related to proteoglycan signaling pathways in angiogenesis and cancer have been identified, including c‑Myc, integrin β1 (ITGB1), Bcl2 and miR‑29a. Therefore, the present study aimed to explore the pathogenesis of IH from the perspective of previously identified miRNA gene network and protein‑protein interactions. Gene and protein levels in human umbilical vein endothelial cells (HUVECs) were analyzed using reverse transcription‑quantitative PCR and western blot (WB) analysis. Cell viability was assessed using a Cell Counting Kit‑8 assay, and the potential association between miR‑29a with ITGB1 was validated using a dual‑luciferase reporter assay. The inhibition of ITGB1 suppressed the β‑catenin/c‑Myc pathway in HUVECs. In addition, transfection with small interfering RNAs (siRNAs) targeting ITGB1 decreased the viability of HUVECs. Furthermore, siRNAs targeting mucin 1 and β‑N‑acetylglucosaminidase significantly inhibited the c‑Myc pathway in HUVECs. The results of WB and dual‑luciferase reporter assays demonstrated that miR‑29a regulated the β‑catenin/c‑Myc pathway and the viability of HUVECs in HUVECs by directly binding to ITGB1. Therefore, miR‑29a may serve as a potential therapeutic target for IH.