Propranolol suppresses infantile hemangioma cell proliferation and promotes apoptosis by upregulating miR-125b expression.

08:00 EDT 1st June 2019 | BioPortfolio

Summary of "Propranolol suppresses infantile hemangioma cell proliferation and promotes apoptosis by upregulating miR-125b expression."

Propranolol could repress infantile hemangioma cell growth and induce apoptosis. miR-125b could inhibit cell proliferation in some tumors. However, whether propranolol exerts its proliferation inhibition and apoptosis-promoting effect by regulating the expression of miR-125b needs to be further investigated. In tumor tissue and endothelial cells isolated from infantile hemangioma patients, we found that the expression levels of miR-125b were significantly decreased. In-vitro analysis revealed that propranolol increased the expression of miR-125b in hemangioma cells in a dose-dependent and time-dependent manner. Interestingly, it was observed that regression of miR-125b expression by its inhibitor could abrogate the effect of propranolol on hemangioma cell growth and apoptosis. In addition, our data further identified TFAP4 as a direct target of miR-125b. Collectively, our data provided evidence that propranolol may repress infantile hemangioma cell growth and promote apoptosis through upregulating the miR-125b expression, which exerted its suppression of tumor development by targeting TFAP4.


Journal Details

This article was published in the following journal.

Name: Anti-cancer drugs
ISSN: 1473-5741
Pages: 501-507


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Medical and Biotech [MESH] Definitions

A proteolytically-cleaved membrane glycoprotein and member of the TNF superfamily that is highly expressed in a variety of tissues including heart, pancreas, brain, and peripheral blood lymphocytes. The secreted extracellular form is a weak inducer of APOPTOSIS for some cell types and a ligand for the FN14 RECEPTOR. It mediates activation of NF-KAPPA-B and promotes ANGIOGENESIS and proliferation of ENDOTHELIAL CELLS, as well as expression of cytokines involved in INFLAMMATION.

The decrease in the cell's ability to proliferate with the passing of time. Each cell is programmed for a certain number of cell divisions and at the end of that time proliferation halts. The cell enters a quiescent state after which it experiences CELL DEATH via the process of APOPTOSIS.

A flavoprotein that functions as a powerful antioxidant in the MITOCHONDRIA and promotes APOPTOSIS when released from the mitochondria. In mammalian cells AIF is released in response to pro-apoptotic protein members of the bcl-2 protein family. It translocates to the CELL NUCLEUS and binds DNA to stimulate CASPASE-independent CHROMATIN condensation.

A dull red, firm, dome-shaped hemangioma, sharply demarcated from surrounding skin, usually located on the head and neck, which grows rapidly and generally undergoes regression and involution without scarring. It is caused by proliferation of immature capillary vessels in active stroma, and is usually present at birth or occurs within the first two or three months of life. (Dorland, 27th ed)

A serine peptidase that contains a C-terminal PDZ domain. It localizes to the mitochondrial membrane and intermembrane space, translocating to the cytoplasm following APOPTOSIS stimuli, such as UV irradiation; it promotes cell death by binding to and inhibiting INHIBITOR OF APOPTOSIS PROTEINS, resulting in an increase in activity of CASPASES. Mutations in the HTRA2 gene are associated with Type 13 PARKINSON DISEASE.

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