[Retracted] Epigenetic silencing of miR­130a ameliorates hemangioma by targeting tissue factor pathway inhibitor 2 through FAK/PI3K/Rac1/mdm2 signaling.

Following the publication of this paper, it was drawn to the authors' attention by an interested reader that some tumours featured in Fig. 6A of the above paper were strikingly similar to those featured in Fig. 8A of an article appearing in the same journal [Fan F­Y, Deng R, Yi H, Sun H­P, Zeng Y, He G­C and Su Y: The inhibitory effect of MEG3/miR­214/AIFM2 axis on the growth of T­cell lymphoblastic lymphoma. Int J Oncol 51: 316­326, 2017]. Furthermore, flow cytometric images featured in Fig. 2G of the above paper were strikingly similar to data featured in the following article [Zhang H­j, Wei Q­f, Wang S­j, Zhang H­j, Zhang X­y, Geng Q, Cui Y­h and Wang X­h: LncRNA HOTAIR alleviates rheumatoid arthritis by targeting miR­138 and inactivating NF­κB pathway. Int Immunopharmacol 50: 283­290, 2017]. The Editor asked the authors for an explanation to account for the appearance of strikingly similar data in their paper independently, and they responded to request that the paper be retracted from International Journal of Oncology. All the authors agreed that the article should be retracted. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 50: 1821­1831, 2017; DOI: 10.3892/ijo.2017.3943].

Epigenetic silencing of miR-130a ameliorates hemangioma by targeting tissue factor pathway inhibitor 2 through FAK/PI3K/Rac1/mdm2 signaling.

Hemangiomas are the most common vascular tumors that occur frequently in prematures and females. microRNA (miR)-130a is associated with the growth and invasion in many tumors, and its role in hemangiomas has not been addressed so far. The present study revealed that miR­130a was overexpressed in infantile hemangioma tissues compared with matched tumor-adjacent tissues. The inhibitor of miR-130a restrained cell growth and induced cell apoptosis in vitro. miR­130a inhibitor also induced a cell cycle arrest at G2/M phase. Further studies revealed that tissue factor pathway inhibitor 2 (TFPI2) was a novel miR-130a target, due to miR-130a bound directly to its 3'-untranslated region and miR-130a inhibitor enhanced the expression of TFPI2. Contrary to the effects of miR-130a inhibitor, TFPI2 siRNA strongly promoted cell growth and colony formation, whereas TFPI2 overexpression contributed to the suppressing effect of miR-130a inhibitor in cell viability. Furthermore, miR-130a inhibitor reduced the activation of focal adhesion kinase (FAK)/phosphoinositide 3-kinase (PI3K)/Rac1/anti-mouse double minute (mdm2) pathway proteins, inhibited the expression and nuclear translocation of mdm2. Moreover, FAK overexpression prevented miR-130a inhibitor-induced cell cycle arrest and decrease of cell viability. In vivo experiments, miR-130a inhibition effectively suppressed the tumor growth, restrained angiogenesis by decreasing the expression of angiogenesis markers and the percentage of CD31+ and CD34+. Taken together, our research indicated that miR-130a functions as an oncogene by targeting TFPI2, miR-130a inhibition reduced the growth and angiogenesis of hemangioma by inactivating the FAK/PI3K/Rac1/mdm2 pathway. Thus, miR-130a may serve as a potential therapeutic strategy for the treatment of hemangioma.

Treatment with propranolol for infantile hemangiomas: A case series of 106 infants.

The aim of the present study was to investigate the clinical benefit and side effects of propranolol treatment in 106 children with infantile hemangiomas (IHs). A retrospective chart review was conducted on all children who attended the clinic between September 16, 2009 and November 11, 2013. Propranolol was administered in a progressive schedule reaching 1.0-1.5 mg/kg/day, divided into three doses. Demographic data, clinical features, imaging, treatment regimens and outcomes were investigated. Any adverse effects following medication were evaluated and managed accordingly. Preliminary analysis of the data showed the inclusion of 106 children (71 female and 35 male) with a mean age and weight at onset of treatment of 5.1 months and 7.3 kg, respectively. All 106 patients responded positively to treatment. Side effects that required intervention and/or close monitoring included diarrhea (n=10), hypotension (n=7), nightmares (n=2), agitation (n=1) and cold extremities (n=1). No long-term adverse effects were observed in any of the patients. In conclusion, propranolol administered orally at 1.0-1.5 mg/kg/day had a rapid therapeutic effect for resolving IHs with few complications.

[Treatment of superficial infantile hemangiomas with topical propranolol].

OBJECTIVE: To evaluate the efficacy and safety of 1% propranolol ointment in the treatment of superficial infantile hemangiomas (IHs). METHODS: A retrospective chart review was performed on 49 children (34 female and 15 male) with a median age of 4.1 months (range, 1-10 months). A total of 58 superficial IHs were treated with 1% propranolol ointment. Topical propranolol was applied three times daily for a mean duration of 21.1 weeks (range, 5-59 weeks). Changes in the size, texture, and color of the tumor were monitored and recorded at regular intervals. The treatment response was evaluated using a 3-point scale system: good, partial, and no response. Adverse effects after medication were evaluated and managed accordingly. RESULTS: Of the 49 cases, 26 (53.1%) demonstrated good response, 17 (34.7%) showed a partial response, and 6 (12.2%) had no response. The total effective rate was 87.8% . No systemic complication was observed in any of the patients. CONCLUSIONS: Topical therapy with 1% propranolol ointment may be a safe and effective method for the treatment of superficial IHs and can be used as an adjuvant treatment measure during the wait-and-see period.

[Oral propranolol in the management of periorbital proliferating phase infantile hemangioma].

OBJECTIVE: To observe the efficacy and safety of oral propranolol in the treatment of periorbital proliferating phase infantile hemangioma. METHODS: A retrospective review of patient medical records was performed. 12 patients (9 female, 3 male; 1.5-8.5 months, average 3.3 months) with periorbital proliferating phase infantile hemangioma underwent oral propranolol therapy. The dosage was slowly increased to 2 mg/kg daily in divided doses for a mean duration of 16 weeks (range 4 weeks-41 weeks). Therapeutic outcomes and safety were established by evaluating colour, size of lesion, duration of treatment and side-effects of treatment before and after treatment. RESULTS: Of these, 9 had a signification reduction in colour and size of the lesions, 2 had no further growth. 1 is stopped therapy due to hypotension after drug administration. 11 other patients, although mild adverse effects were noted, no symptoms were severe enough to discontinue treatment. CONCLUSIONS: Propranolol appears to be a safe and effective treatment in the management of periorbital proliferating phase infantile hemangioma.

[The change of serum vascular endothelial growth factor and matrix metalloproteinases-9 in proliferative hemangioma treated with propranolol].

OBJECTIVE: To study the level of serum vascular endothelial growth factor, matrix metalloproteinases-9 in the proliferative hemangioma before and after propranolol treatment. METHODS: The serum VEGF, MMP-9 was detected with ELISA assay before treatment and after 4 weeks and 8 weeks of propranolol treatment. The relationship between the serum VEGF, MMP-9 and the prognosis was analyzed. RESULTS: The serum VEGF (295.4 +/- 158.1) pg/ml was high before treatment, then decreased after 4 weeks and 8 weeks of treatment (255.7 +/- 130.4) pg/ml, (224.2 +/- 120.6) pg/ml. The serum VEGF was significantly lower after 8 weeks of treatment (P < 0.05). The serum MMP-9 was also decreased after treatment, showing a positive relationship with VEGF. CONCLUSIONS: Propranolol can treat the proliferative hemangioma through decreasing the serum VEGF and MMP-9.

[The expression of CEACAM-1 and CXCL-14 in infantile hemangioma].

OBJECTIVE: To examine the expression of CEACAM-land CXCL-14 in the different stages of infantile hemangioma and to explore the role of CEACAM-1 and CXCL-14 in the occurrence and development of infantile hemangioma. METHODS: The expression of CEACAM-1 and CXCL-14 was detected by immunohistochemical technique and Western Blot in cases of proliferating hemangiomas, involuting hemangiomas, involuted hemangiomas. The mean optical density was measured by image analysis system. RESULTS: The expression of CEACAM-1 in early stage of proliferating hemangiomas was weak or negative, while it was strong in involuting hemangiomas and positive in the involuted stage. The differences between different stages had a statistically significance (P < 0.05). The expression of CXCL-14 was weak or negative in stage of proliferating hemangiomas, positive in involuting hemangiomas and strong in the involuted stage. The differences between different stages had a statistically significance (P < 0.05). CONCLUSIONS: CEACAM-1 and CXCL-14 are involved in the occurrence and development of infantile hemangioma.