Mechanisms of Action of MicroRNAs in Infantile Hemangioma Tissue and Vascular Endothelial Cells in Different Periods

Chen, Junjiang; Li, Chen; Li, Yuqiang; Wang, Yu

doi:10.12659/msm.902374

Cited by 6 publications

(4 citation statements)

References 23 publications

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“…MiRNAs are involved in the development and disorders of hemangioma. For example, miR-29a, miR-206, and miR-455 participate in a variety of biological functions at different stages of IHA (13). The role of miR-424 in IHA has also been widely reported.…”

Section: Discussionmentioning

confidence: 99%

Propranolol inhibits infantile hemangioma by regulating the miR-424/vascular endothelial growth factor-A (VEGFA) axis

Wu¹,

Shi²,

Pan³

et al. 2021

Transl Pediatr

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Background: Infantile hemangioma (IHA) is the most common tumor in infancy. We aimed to explore the effect of propranolol on the expression of microRNA (miR)-424 in IHA tissues and XPTS-1 cells, as well as its molecular mechanism of inhibiting XPTS-1 cell activity.Methods: Tumor tissues and peritumoral tissue were collected from 13 IHA patients in Lishui Municipal Central Hospital. The level of miR-424 were detected using real-time quantitative reverse transcription polymerase chain reaction (RT-PCR). Cell counting kit-8 (CCK-8) was used to measure XPTS-1 cell viability. Flow cytometry and transwell were used to detect the apoptosis level and invasion ability of XPTS-1 cells. Western blot was used to measure the protein level of vascular endothelial growth factor-A (VEGFA).The luciferase reporter gene assay detected the targeting relationship between miR-424 and VEGFA. Results: Compared with normal tissues and human umbilical vein endothelial cells, the expression level of miR-424 in IHA tissues and XPTS-1 cells was significantly reduced (P<0.05). As the concentration of propranolol increased, XPTS-1 cell viability gradually decreased (P<0.05), and the expression level of VEGFA decreased (P<0.05). The expression of miR-424 increased with the time of propranolol treatment (P<0.05). Compared with the control group, treatment with an miR-424 inhibitor resulted in a significant increase in XPTS-1 cell viability and invasion ability (P<0.05), and a decrease in apoptosis (P<0.05). However, both propranolol and miR-424 inhibitor treatment resulted in a partial decrease in XPTS-1 cell viability (P<0.05), and a partial increase in the level of apoptosis (P<0.05). MiR-424 directly targeted VEGFA; the overexpression of miR-424 resulted in a decrease in the VEGFA protein level (P<0.05), while inhibition of miR-424 resulted in an increase in the VEGFA protein level (P<0.05). Compared with the propranolol group, the XPTS-1 cell viability and invasion ability in the propranolol + VEGFA-si group were significantly decreased (P<0.05), while the level of apoptosis increased (P<0.05). Meanwhile, simultaneous miR-424 inhibitor treatment resulted in no difference in cell viability and apoptosis levels compared with the propranolol group, and the invasion ability was partially restored (P<0.05). Conclusions: Propranolol affects the malignant biological behavior of IHA cells by regulating the miR-424/VEGFA axis.

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Section: Discussionmentioning

confidence: 99%

Propranolol inhibits infantile hemangioma by regulating the miR-424/vascular endothelial growth factor-A (VEGFA) axis

Wu¹,

Shi²,

Pan³

et al. 2021

Transl Pediatr

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“…There are many factors affecting the proliferation, migration, and apoptosis of HemECs. Some studies have shown that VEGF, 14,17 microRNA (miRNA), 18,19 long noncoding RNAs (lncRNAs), 3 and other various molecules are abnormally expressed in IH. MicroRNA is a member of a small RNA family of approximately 20 nucleotides that functions by modulating mRNA 20 .…”

Section: Hemangioma Ecs In Ihmentioning

confidence: 99%

“…The expression of miR-424 in the proliferating phase of IH is lower than the involuting phase, and overexpression of miR-424 suppresses the proliferation and migration of HemECs by targeting FGFR1 to inhibit the signal pathway of basic fibroblast growth factor/FGFR1, which results in the downregulation of ERK1/2 phosphorylation level 43 . Chen et al 19 have found that miR-29a, miRNA-206, and miRNA-455 expressed differently at different stages of IH. They believed that miRNA-206 played a role in the regression of IH by regulating the proliferation and migration of HemECs, but the specific mechanism was unclear.…”

Section: Hemangioma Ecs In Ihmentioning

confidence: 99%

Hemangioma Endothelial Cells and Hemangioma Stem Cells in Infantile Hemangioma

Sun

Qiu

et al. 2022

Ann Plast Surg

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Background: Hemangioma is one of the most common benign tumors in infants and young children. The 2 most important cells in the course of infantile hemangioma (IH) are hemangioma stem cells (HemSCs) and hemangioma endothelial cells (HemECs). Infantile hemangioma is characterized by massive proliferation of HemECs, but current studies indicate that HemSCs play an important role in pathogenesis of IH.Objective: This review aimed to identify molecules that influence HemSC differentiation and HemEC proliferation and apoptosis to help clarify the pathogenesis of IH and provide novel drug targets for the treatment of IH. Methods: Relevant basic science studies related to IH were identified by searching Google Scholar, Embase, PubMed, MEDLINE, and peer-reviewed journal articles. Result: Hemangioma stem cells can differentiate into HemECs, pericytes, and adipocytes. In the proliferating phase of IH, HemSCs mainly differentiate into HemECs and pericytes to promote angiogenesis. In the regressive phase, they mainly differentiate into adipocytes. Therefore, increasing the proportion of HemSCs differentiating into adipocytes, inhibiting the proliferation of HemECs, and promoting the apoptosis of HemECs can facilitate the regression of IH.

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“…In addition to the lncRNAs, microRNAs (miRNAs), a subgroup of ncRNAs with about 20 nucleotides that inhibit their target gene are differentially expressed in different phase HAs [19]. Some studies showed that miR-143, miR-199a and miR-130a are involved in regulating cell proliferation and invasion in HAs cells [20][21][22].…”

Section: Introductionmentioning

confidence: 99%

lncRNA MEG3 Suppresses the Tumorigenesis of Hemangioma by Sponging miR-494 and Regulating PTEN/ PI3K/AKT Pathway

Dai

Wan

Qiu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Dysregulation of long noncoding RNAs (lncRNAs) is associated with the proliferation and metastasis in a variety of cancers, of which lncRNA maternally expressed gene 3 (MEG3) has been indicated as a tumor suppressor in multiple malignancies. However, the underlying mechanisms by which MEG3 contributes to human hemangiomas (HAs) remain undetermined. Methods: qRT-PCR analysis was performed to examine the expression levels of MEG3 and VEGF in proliferating or involuting phase HAs. MTT, colony formation assay, flow cytometry analysis and a subcutaneous xenograft tumor model were conducted to assess the effects of MEG3 on the HAs tumorigenesis. The interaction between MEG3 and miRNAs or their downstream pathways was evidenced by bioinformatic analysis, luciferase report assays, RNA immunoprecipitation (RIP) assay. and Western blot analysis. Results: The expression of MEG3 was substantially decreased and had a negative correlation with VEGF expression in proliferating phase HAs, as compared with the involuting phase HAs and normal skin tissues. Ectopic expression of MEG3 suppressed cell proliferation, colony formation and induced cycle arrest in vitro and in vivo, followed by the downregulation of VEGF and cyclinD1, but knockdown of MEG3 reversed these effects. Furthermore, MEG3 was verified to act as a sponge of miR-494 in HAs cells, and miR-494 counteracted MEG3-caused anti-proliferative effects by regulating PTEN/PI3K/AKT pathway, and exhibited the negative correlation with MEG3 and PTEN expression in proliferating phase HAs. Conclusion: Our findings suggested that lncRNA MEG3 inhibited HAs tumorigenesis by sponging miR-494 and regulating PTEN/PI3K/AKT pathway.

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Mechanisms of Action of MicroRNAs in Infantile Hemangioma Tissue and Vascular Endothelial Cells in Different Periods

Cited by 6 publications

References 23 publications

Propranolol inhibits infantile hemangioma by regulating the miR-424/vascular endothelial growth factor-A (VEGFA) axis

Propranolol inhibits infantile hemangioma by regulating the miR-424/vascular endothelial growth factor-A (VEGFA) axis

Hemangioma Endothelial Cells and Hemangioma Stem Cells in Infantile Hemangioma

lncRNA MEG3 Suppresses the Tumorigenesis of Hemangioma by Sponging miR-494 and Regulating PTEN/ PI3K/AKT Pathway

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